Chapter 10: Human Health and Diseases
In the closing years of the nineteenth century, a British army doctor named Ronald Ross was posted in India, working in Secunderabad. Malaria was everywhere around him. Villages emptied during fever season, soldiers collapsed in their barracks, and nobody could say for certain how the disease travelled from one person to the next. Bad air rising from swamps was the popular explanation — the word “malaria” itself means “bad air”.
Ross suspected the mosquito instead. He spent long, frustrating months letting mosquitoes feed on infected patients, then dissecting the insects one by one under a microscope in the heat of an Indian summer. Most dissections showed nothing. Then, in a mosquito he had reared himself, he found dark-pigmented cysts in the stomach wall — the malaria parasite, alive and developing inside the insect. The chain was complete: parasite, mosquito, human. For this work he was awarded a Nobel Prize.
That single observation changed public health forever. It showed that a disease is not a punishment or a mystery — it is a biological process, with a cause, a carrier, a route of entry, and therefore a point where it can be broken.
This chapter is about exactly that: how pathogens reach us, how our body fights back, why some diseases strike only once, and how our own choices shape our health.
Diagram
Fig. 10.0 – A researcher at a microscope beside a magnified inset showing a mosquito taking a blood meal from human skin, with the parasite passing from mosquito to human; label mosquito (vector), human (host), parasite (pathogen).
By the end of this chapter, you will be able to answer each of these questions yourself.
10.1 Immunity
What Health Really Means
Most of us use the word “health” loosely, as if it simply means “not being ill”. Health is actually much wider than that. It is not merely the absence of disease, and it is not only physical fitness either.
The World Health Organization (WHO) defines health as a state of complete physical, mental and social well-being, and not merely the absence of disease or infirmity. Notice how three different levels are packed into that one sentence: the body must work well, the mind must be at ease, and the person must be able to live and function within society. In this sense, health is a birth right of every human being.
Health also reflects the metabolic and functional efficiency of a living organism. In other words, a healthy body is one in which the chemical reactions of metabolism and the working of organs are proceeding smoothly and efficiently. This is why health is a biological idea and not only a social one.
Hygiene is the science of the rules of health — the set of practices that keep our body and our surroundings free of disease-causing organisms. Achieving good health therefore needs several things together: a hygienic balanced diet, clean drinking water, personal and community hygiene, regular physical exercise, knowledge about diseases and their effects on the body, proper disposal of waste, and control of vectors (the organisms that carry pathogens from one person to another).
Why We Usually Stay Healthy
Every single day we are exposed to foreign bodies — dust, pollen, and infectious agents such as bacteria and viruses. They land on our skin, enter with our food, and are drawn in with every breath.
Yet despite this constant exposure to a wide variety of pathogens, most of us remain healthy most of the time. The reason is that the human body is able to resist almost every type of foreign body that reaches it. This resistance is not luck; it is the work of a dedicated defence network.
The system that protects us from various infectious agents is called the immune system. Resistance is the ability to prevent damage or disease through this defence mechanism. The rest of this section is about how that system recognises an enemy, and how it destroys it.
The Meaning of Immunity
The term “immunity” has traditionally referred to the resistance shown by a host towards injury caused by pathogens and their products. Protection against infectious disease, however, is only one of the many consequences of the immune response. The immune response, in the fullest sense, is the body’s reaction against any foreign antigen — whether it comes from a germ, a transplanted organ, or a grain of pollen.
The word “immunity” itself carries the sense of “freedom” or “exempt” — a person who is immune is, in effect, exempt from that particular disease. The concept of immunity is believed to have started with Edward Jenner in England, who developed the cowpox vaccine to protect against attack by small pox (a virus).
The branch of science that deals with the study of the immune system, immune responses to foreign substances, and their role in resisting infection by pathogens, is called Immunology.
Self and Non-Self: The Central Skill of the Immune System
The most important characteristic of the immune system is that it distinguishes self (the body’s own cells) from non-self (foreign molecules or invading cells). Every cell of your body carries surface molecules that act like an identity card; the immune system reads these cards constantly.
This ability matters enormously. If the system could not tell self from non-self, it would either ignore invaders (and we would die of infection) or attack our own tissues (which is what happens in autoimmune disease). So the immune system differentiates between the body’s own cells and the invaders.
Any foreign substance that invades the body and is capable of stimulating an immune response is called an antigen. The protective chemicals produced by immune cells in response to antigens are called antibodies.
Types of Immunity
There are two types of immunity: Innate or Inborn (inherited) immunity, and Acquired or Adaptive immunity. The whole scheme of immunity, with all its branches, is summarised in FC 10.1.
Flowchart
FC 10.1 – Types of immunity: Immunity → (A) Innate/Inborn immunity → epithelial barriers → antimicrobial substances in blood and tissues → cellular factors → fever → acute phase proteins; and (B) Acquired/Adaptive immunity → Active immunity → natural (infection) or artificial (vaccine); and Passive immunity → natural (placenta, colostrum) or artificial (readymade antibodies in serum)
Innate Immunity or Inborn Immunity
Innate immunity is the resistance to infection that an individual possesses by virtue of his or her genetic make-up. You are born with it. It is the natural (inborn) defence system of the body, and it is not affected by prior contact with microorganisms or by immunisation — it works the very first time a germ arrives, exactly as it works the hundredth time.
Innate immunity is non-specific when it gives a general degree of resistance to infection as a whole, and specific when the resistance concerns one particular pathogen. Most of it, though, is of the general kind: a set of defences that does not care which germ has arrived, only that something foreign is present.
One form of innate immunity comprises the various types of barriers that prevent the entry of foreign agents into the body. Think of these as the walls and gates of a fort — they act before any fighting begins inside.
a. Epithelial surfaces
The intact skin and the mucous membranes covering the body protect it considerably against invasion by microorganisms. As long as they are unbroken, they form a continuous physical sheet that most germs simply cannot cross. The main surface defences are shown in Fig. 10.15.
Diagram
Fig. 10.15 – Barriers of innate immunity in the human body; label skin (salt in drying sweat, sebaceous secretions), tears (lysozyme), nasal hair and mucus, cough reflex in trachea, saliva in mouth, acidic gastric secretions in stomach, flushing action of urine, spermine and zinc in semen.
Healthy skin possesses bactericidal activity because of the high concentration of salt in drying sweat — as sweat dries, salt is left behind, and few bacteria survive on such a salty surface. Sebaceous (oil gland) secretions and long-chain fatty acids have bactericidal and fungicidal properties, killing bacteria and fungi respectively.
The mucosa of the respiratory tract has several innate mechanisms of defence. The nose prevents the entry of microorganisms to a large extent: inhaled particles are arrested by the hair at or near the nasal orifices. Those that pass beyond are held by the mucus lining the epithelium and are swept back to the pharynx, where they tend to be swallowed or coughed out. The cough reflex is itself an important defence mechanism of the respiratory tract — it is a forced expulsion that clears trapped particles.
The mouth is constantly bathed in saliva, which has an inhibitory effect on microorganisms. The acidity of the gastric secretions in the stomach destroys microorganisms that arrive with food or with swallowed mucus. The flushing action of urine eliminates bacteria from the urethra — the constant downward flow simply does not allow them to settle. Spermine and zinc present in semen are antibacterial.
b. Antimicrobial substances in blood and tissues
If a pathogen does get past the barriers, it meets a second line of innate defence — chemicals already circulating in the blood and tissues.
The complement system contains more than 30 serum proteins that circulate in the blood in an inactive state. They are, in effect, loaded weapons kept on safety. The presence of microbial pathogens activates the “Complement cascade” — one protein activates the next, which activates the next — and the end result is the elimination of the pathogen. A cascade is used because it amplifies the signal: a small trigger produces a very large response, very fast.
The interferons are a class of cytokines (soluble proteins) released by cells infected with viruses and by certain white blood cells. Interferons stimulate other cells to protect themselves from viral infection. Notice the logic here: an infected cell may not be able to save itself, but before it dies it can warn its neighbours — and that warning is what limits the spread of a virus through a tissue.
c. Cellular factors in innate immunity
Natural defence against the invasion of blood and tissues by microorganisms and other foreign particles is mediated to a large extent by phagocytic cells, which ingest and destroy them. Phagocytic cells were discovered by Metchnikoff in 1882. They are grouped as microphages and macrophages, and they remove foreign particles that enter the body.
A class of lymphocytes called Natural killer (NK) cells is important in the non-specific defence against viral infections and tumours. NK cells do not wait to be told which cell to kill; they detect body cells that have “gone wrong” — virus-infected or cancerous — and destroy them directly.
d. Fever
An increase in body temperature following an infection is itself a natural defence mechanism. Fever is not the disease; it is part of the response to the disease.
A raised temperature helps in two ways. It accelerates the physiological processes that destroy the invading pathogens, and it stimulates the production of interferon, which helps in recovery from viral infections. Many pathogens also grow poorly above the normal body temperature, so the fever makes the body a less comfortable place for them.
e. Acute phase proteins (APPs)
Infection or injury leads to a sudden increase in the concentration of certain plasma proteins, collectively called acute phase proteins. These include C Reactive Protein (CRP), Mannose binding protein, Alpha-1-acid glycoprotein, Serum Amyloid P, and others.
APPs are believed to enhance host resistance, prevent tissue injury, and promote the repair of inflammatory lesions. Because their level rises sharply and quickly, doctors often measure CRP in the blood as a simple indicator that inflammation or infection is present somewhere in the body.
Acquired Immunity
The resistance that an individual acquires during life is known as acquired immunity. It is also known as adaptive or specific immunity. It involves the formation of antibodies in the body, which neutralise the antigens.
Acquired or adaptive immunity has four unique features, and each one is worth understanding rather than memorising:
a. Specificity: It can produce a specific antibody or a specific T-lymphocyte against a particular antigen or pathogen. One antibody, one antigen — like one key for one lock.
b. Diversity: It can recognise a vast variety of diverse pathogens or foreign molecules, including ones the body has never met before.
c. Discrimination between self and non-self: It differentiates between the body’s own cells (self) and foreign (non-self) molecules — the same central skill described earlier, now applied with precision.
d. Memory: When the immune system encounters a specific foreign agent for the first time, it generates an immune response and eliminates the invader. This is called the first encounter. The immune system retains the memory of this first encounter. As a result, a second encounter with the same pathogen brings about a quicker and stronger immune response.
Memory is the feature that makes vaccination possible at all. Without it, every exposure to a germ would be as dangerous as the first.
Types of Acquired Immunity
Acquired immunity is of two types — Active and Passive.
a. Active immunity
Active immunity is the resistance developed by an individual as a result of an antigenic stimulus. It is also known as adaptive immunity. The key word here is developed: the person’s own immune system does the work, makes the antibodies, and forms the memory cells. That is why active immunity takes time to appear but lasts long. Active immunity may be natural or artificial.
1. Naturally acquired active immunity: Immunity acquired due to infection is called natural active immunity. It develops after the entry of pathogens into the body. It is long-lasting immunity. For example, a person who has recovered from an attack of measles develops naturally acquired active immunity to measles for a lifetime.
2. Artificially acquired active immunity: This is the resistance induced by vaccines. A vaccine is introduced into the body to stimulate the formation of antibodies by the immune system — for example, polio vaccine and BCG vaccine. Such immunity may be temporary or permanent.
b. Passive immunity
Passive immunity is acquired when readymade antibodies are received by the body cells — that is, the body’s own cells take no active part in the production of immunity. Somebody else’s antibodies are simply handed over. This is why passive immunity acts immediately but is always short lived: the borrowed antibodies are gradually broken down, and since no memory cells were formed, nothing is left behind. Passive immunity can be acquired either naturally or artificially.
1. Naturally acquired passive immunity: Before birth, maternal antibodies are transferred from the mother to the foetus through the placenta. After birth, antibodies are transferred from mother to infant through colostrum (the first milk of the mother) and continue throughout the period of breast feeding. The antibodies received by the baby from the mother remain in the body for a short time. Therefore, naturally acquired passive immunity is short lived.
2. Artificially acquired passive immunity: This immunity is developed by injecting previously prepared antibodies, using serum from humans or animals. For example, antibodies obtained from hyper-immunised horses are injected into humans against rabies pathogens. It is short lived.
Cells of the Immune System
There are two main types of cells involved in the working of the immune system: (a) Lymphocytes, and (b) Antigen presenting cells.
a. Lymphocytes
Lymphocytes are the main cells of the immune system. Like the other blood corpuscles, they arise from the stem cells, the haemocytoblasts, present in the liver of the foetus and in the bone marrow in the adult.
From this common origin, they take two different training routes, and this is what decides what kind of cell they become. Some of them undergo differentiation in the gut-associated bursal lymphoid tissues (tonsils, Peyer’s patches) and are called Bursal or B-lymphocytes. Others are differentiated in the thymus gland and are termed T-lymphocytes. The origin and differentiation of the two lines is shown in Fig. 10.16.
Diagram
Fig. 10.16 – Origin and differentiation of lymphocytes; label haemocytoblast (stem cell) in foetal liver / adult bone marrow, branch to gut-associated bursal lymphoid tissue (tonsils, Peyer’s patches) → B-lymphocyte → AMIS, and branch to thymus gland → T-lymphocyte → CMIS.
The mature lymphocytes pass into the body fluids (blood and lymph) and circulate in the body. Many of them stay in the lymph nodes, which act as checkpoints where circulating antigens are likely to be caught.
The B-lymphocytes and T-lymphocytes form the humoral or antibody-mediated immune system (AMIS) and the cell-mediated immune system (CMIS) respectively. Both immune systems need antigens to come into action, but they respond in different ways: B-cells send out antibodies into the body fluids, while T-cells act through the cells themselves.
Mechanism of response of T-lymphocytes to antigens
On coming in contact with an antigen, a T-lymphocyte forms clones of T-cells. All the cells of a clone are similar, but they perform different functions. The clone has four types of T-lymphocytes, as traced in FC 10.2.
Flowchart
FC 10.2 – T-cell response: antigen contact → T-lymphocyte activated → forms a clone of T-cells → branches into (i) Helper T-cells → secrete lymphokines → stimulate other T-cells, B-lymphocytes and macrophages; (ii) Killer/Cytotoxic T-cells → secrete perforins → hole in infected cell → cell killed; (iii) Suppressor T-cells → switch off the response against self; (iv) Memory T-cells → retain sensitisation for a future encounter
i. Helper T-cells: Sensitised helper T-cells produce lymphokines, which perform several types of functions such as the proliferation of other T-cells and the stimulation of B-lymphocytes, macrophages, and so on. They are the coordinators of the response — they do not kill, they instruct.
ii. Killer T-cells or Cytotoxic T-cells: They directly attack and destroy invading microbes, infected body cells, and cancer cells. Killer T-cells bind to the infected cell and secrete perforins. The perforins then form a hole in the infected cell. The killer cell also releases substances that kill the cell — hence the name cytotoxic (“cell-poisoning”) T-cell.
iii. Suppressor T-cells: These cells suppress the entire immune system against an attack on the body’s own cells. They act as the brake, protecting “self” from a response meant for “non-self”.
iv. Memory T-cells: These are previously sensitised cells which retain the memory of sensitisation for a long time in the future. They are the reason the second encounter is faster than the first.
Mechanism of action of B-lymphocytes to antigens
B-lymphocytes are sensitised directly by antigens as well as by helper T-cells — so they can be triggered either by meeting the enemy themselves or by receiving instructions.
An activated B-lymphocyte multiplies very fast to produce a clone of plasma cells and memory B-cells. The plasma cells produce specialised glycoproteins, called antibodies, which are circulated through body fluids (humor) such as blood and lymph — this is why the B-cell system is called the humoral or antibody-mediated system. The antibody molecules may bind to a cell membrane, or they may remain free. The whole sequence is shown in FC 10.3.
Flowchart
FC 10.3 – B-cell response: antigen (directly, or via helper T-cell) → B-lymphocyte sensitised → rapid multiplication → clone of plasma cells + memory B-cells → plasma cells secrete antibodies into blood and lymph → antibodies act by agglutination, opsonisation and neutralization; memory B-cells remain for a faster second response
The free antibodies have three main functions:
i. Agglutination of particulate matter, including bacteria and viruses. The antibodies clump the particles together into an immobilised mass, which is then engulfed by phagocytes. Clumping is useful because one phagocyte can now swallow many bacteria at once instead of chasing each one.
ii. Opsonisation, or the coating of bacteria to facilitate their subsequent phagocytosis by macrophages. The coating acts like a handle that the macrophage can grip.
iii. Neutralization of toxins released by bacteria — for example, tetanus toxin. Here the antibody does not kill the bacterium at all; it binds and blocks the poison the bacterium has released.
The three functions of free antibodies are compared in Fig. 10.17. And in every one of them, the same rule applies: each antibody is specific for a particular antigen.
Diagram
Fig. 10.17 – Three functions of free antibodies; label (a) agglutination — antibodies clumping bacteria into an immobilised mass engulfed by a phagocyte, (b) opsonisation — antibodies coating a bacterium which is then gripped by a macrophage, (c) neutralization — antibodies binding a bacterial toxin molecule and blocking it.
b. Antigen Presenting cells
Antigen presenting cells engulf invading pathogens and process the antigens. The processed antigens are then presented on the cells’ own surface, like an exhibit held up for inspection.
This step is not a formality. These cells are able to deliver a stimulatory signal that is necessary for the activation of helper T-cells. In other words, a helper T-cell usually cannot recognise a free-floating pathogen on its own — the antigen must first be caught, cut up, and displayed for it. The process is shown in Fig. 10.18.
Diagram
Fig. 10.18 – An antigen presenting cell engulfing a bacterium, processing the antigen inside, displaying the processed antigen fragment on its surface, and delivering a stimulatory signal to a helper T-cell.
Vaccination
The administration of a vaccine — that is, an inactivated pathogen, or the antigenic protein of a particular pathogen — to protect against that particular pathogen, is called vaccination.
The body’s immune system helps to protect us against pathogens that cause infection. It is an efficient system most of the time: it either keeps microorganisms out, or tracks them down and gets rid of them. However, some pathogens can overwhelm the immune system, and when this happens it can cause serious illness. The pathogens most likely to cause problems are the ones the body does not recognise — because recognition is the first step of every specific response.
Vaccination is a way to “teach” the immune system how to recognise and eliminate a pathogenic organism, in advance. That way, the body is always prepared if you are ever exposed. Notice that this is simply the memory feature of acquired immunity, put to deliberate use. The idea is summarised in FC 10.4.
Flowchart
FC 10.4 – How vaccination works: vaccine (killed / attenuated pathogen, toxoid, or antigenic protein) → antigen recognised by immune system → B-cells activated → antibodies produced + memory cells formed → later, the real pathogen enters → memory cells respond quickly and strongly → pathogen eliminated before disease develops
Vaccination is an important form of primary prevention — prevention that stops a person from getting sick in the first place, rather than treating them afterwards. Vaccination has allowed us to control diseases such as measles, polio, tetanus and whooping cough, which once threatened many lives.
It is important that as many people as possible get vaccinated. Vaccinations do not just protect individuals: when enough people in a community are vaccinated, the pathogen finds too few susceptible bodies to spread through, and so the whole society is protected — including those who cannot be vaccinated, such as very young infants.
Vaccinations are safe. Vaccines are considered to be safe. They are rigorously tested and go through many rounds of study, examination and research before they are used for the general public. Extensive research and evidence show that vaccines are safe, and that their side effects are rare and typically mild.
10.2 Structure of Antibody
Antibodies are glycoproteins — proteins carrying carbohydrate chains — and each of them is highly specific to one particular antigen. They are also known as Immunoglobulins (Igs), and they are produced in response to antigenic stimulation. In other words, an antibody is never made “in advance and in general”; it is made because a particular antigen has arrived.
You already know that antibodies are produced by plasma cells, which are in turn formed from B-lymphocytes. What is worth noting is the sheer speed of the factory: a mature plasma cell produces antibodies at the extremely rapid rate of about 2000 molecules per second. This is why the body can flood the blood and lymph with a specific antibody within days of an infection.
The Shape of an Antibody Molecule
An antibody is a ‘Y’ shaped molecule. Each immunoglobulin molecule is made up of four polypeptide chains: two heavy or H-chains and two light or L-chains. The general plan is shown in Fig. 10.1.
Diagram
Fig. 10.1 – Structure of antibody: Y-shaped molecule; label two heavy (H) chains, two light (L) chains, disulfide bonds (-s-s-), hinge region, variable region of heavy chain, variable region of light chain, constant region of heavy chain, constant region of light chain, and the two antigen binding sites (paratopes) at the tips of the arms, with N and C ends of the chains marked.
The four polypeptide chains are held together by disulfide bonds (-s-s-) to form the ‘Y’ shaped structure. A disulfide bond is a strong covalent link between two sulphur atoms, and it is what stops the four separate chains from drifting apart. The region that holds together the arms and the stem of the antibody is termed the hinge. As the name suggests, it allows the two arms to swing a little — which lets a single antibody grip two antigen particles that are not perfectly aligned.
Each chain of the antibody includes two distinct regions: the variable region and the constant region. The constant region is much the same in all antibodies of a class; the variable region differs from antibody to antibody.
Variable regions constitute the antigen-binding site, called the paratope. This part of the antibody recognises and binds to the specific antigen to form an antigen-antibody complex. Since most antibodies carry two antigen binding sites — one at the tip of each arm — they are said to be bivalent.
Formation of the Antigen–Antibody Complex
The study of antigen-antibody interactions is called serology. This is the science behind blood grouping, the diagnosis of infections, and many laboratory tests you will meet later in this chapter.
Each antibody is specific for a particular antigen. The combining sites of an antigen are called antigenic determinants or epitopes. These epitopes react with the corresponding antigen binding sites of antibodies, called paratopes. Fig. 10.2 shows how several antibodies bind to the epitopes on the surface of a virus.
Diagram
Fig. 10.2 – Formation of antigen–antibody complex: a virus particle with antigenic determinants (epitopes) on its surface, paratopes of antibodies bound to those epitopes; also show free antigens with globular proteins bound to antibodies.
The antigen binding sites (paratopes) are located on the variable regions of the antibody. Small variations in these variable regions make each antibody highly specific for a particular antigen. The variable region enables the antibody to recognise the specific antigen and to bind to it in a lock and key manner, forming an antigen-antibody complex.
Antigens on Blood Cells
So far we have talked about antigens as things that come from outside. But antigens also sit on the surface of our own cells — and on red blood cells they have a very practical consequence.
There are several known antigens on the surface of human red blood cells. These antigens give rise to the different blood groups. There are many genetically determined blood group systems, such as ABO, Rh, Duffy, Kidd, Lewis, P, MNS and the Bombay blood group. “Genetically determined” is the key phrase: a person does not acquire a blood group during life — it is inherited, like eye colour.
ABO Blood Groups
The A, B and O blood groups were discovered by Karl Landsteiner in 1900. Later on, the blood group AB was discovered by Landsteiner’s students Decastello and Sturli in 1902. Landsteiner was awarded the Nobel Prize for his discovery of human blood groups.
He found two antigens, or agglutinogens, on the surface of human red blood cells, and named them antigen A and antigen B. He also noticed the corresponding antibodies, or agglutinins, in the serum, called ‘a’ and ‘b’.
In the ABO system, the blood groups are determined by the presence or absence of antigen A and antigen B. On this basis, a person’s blood group is classified into four groups: A, B, AB and O.
Blood group A: Individuals with blood group ‘A’ have the antigen A on the surface of their red blood cells (RBCs), and antibody ‘b’ in their plasma.
Blood group B: Individuals with blood group ‘B’ have the antigen B on the surface of their RBCs, and antibody ‘a’ in their plasma.
Blood group AB: Individuals with blood group ‘AB’ have both antigens A and B on the surface of their RBCs, and no antibodies in their plasma.
Blood group O: Individuals with blood group ‘O’ lack both antigens A and B on the surface of their RBCs, and show the presence of both ‘a’ and ‘b’ antibodies in their plasma.
Look carefully at the pattern. A person never carries the antibody against his or her own antigen — if they did, their own immune system would clump their own red cells. This is the self/non-self rule from the previous section, written into our blood.
Table 10.3 sets out the whole system, including the genotypes, in one place.
Table 10.3: ABO Blood groups in man
| Blood group | Genotype | Antigen on surface of RBC | Antibody in serum | Can donate blood to | Can receive blood from |
|---|---|---|---|---|---|
| A | \(I^A I^A\) or \(I^A I^O\) | A | Antibody b | A, AB | A, O |
| B | \(I^B I^B\) or \(I^B I^O\) | B | Antibody a | B, AB | B, O |
| AB (universal acceptor) | \(I^A I^B\) | A and B | Nil | AB | A, B, AB, O |
| O (universal donor) | \(I^O I^O\) | Nil | Both Antibody a and Antibody b | A, B, AB, O | O |
Rh Factor
Rh is the most complex of the blood group systems. The Rh factor is an antigenic protein present on the surface of the red blood cells in human beings.
It was first discovered by Landsteiner and Wiener (1940) on the surface of the RBCs of the Rhesus monkey — which is why it is called the Rh factor. It is also called the D antigen. A person having the Rh factor (D antigen) is called Rh positive (Rh +ve), and one lacking the D antigen is called Rh negative (Rh -ve).
The Rh (D) antigen induces a strong immunogenic response when introduced into Rh -ve individuals. That is, an Rh -ve person’s immune system treats the D antigen as a genuine foreigner and makes antibodies against it. The Rh blood group is therefore an important factor in blood transfusion, and it is involved in haemolytic disease of the newborn (HDN), which is called erythroblastosis foetalis (destruction of the erythrocytes of the foetus). It occurs when an Rh -ve mother conceives an Rh +ve foetus.
How erythroblastosis foetalis develops
The Rh +ve RBCs from the foetus may enter the mother’s circulatory system during childbirth, causing her to produce anti-Rh antibodies. Note the timing: this usually happens at delivery, so the first Rh +ve baby is generally born unharmed — the mother’s immune system is being sensitised only as that baby is born.
As a result, subsequent Rh +ve foetuses will be exposed to the anti-Rh antibodies produced by the mother. These antibodies cross into the foetal circulation and destroy the foetal red blood cells, which results in HDN. The sequence is set out in FC 10.5.
Flowchart
FC 10.5 – Erythroblastosis foetalis: Rh -ve mother conceives Rh +ve foetus → at childbirth, Rh +ve foetal RBCs enter mother’s circulation → mother produces anti-Rh antibodies (mother is now sensitised) → in a subsequent Rh +ve pregnancy, these anti-Rh antibodies reach the foetus → foetal RBCs are destroyed (haemolysis) → haemolytic disease of the newborn (erythroblastosis foetalis)
In order to prevent HDN, the Rh -ve mother is injected with the anti-Rh antibody during all pregnancies carrying an Rh +ve foetus. The idea behind this looks strange at first — we are giving her the very antibody we are afraid of — but the logic is sound: the injected readymade antibodies destroy the stray foetal Rh +ve cells before the mother’s own immune system can register them and start making its own antibodies. She therefore never becomes sensitised, and her later babies are safe. This is a use of passive immunity to prevent an unwanted active immune response. Fig. 10.19 compares the sensitised and the protected pregnancy.
Diagram
Fig. 10.19 – Rh incompatibility: (a) first pregnancy — Rh -ve mother, Rh +ve foetus, foetal RBCs entering maternal blood at delivery, mother forming anti-Rh antibodies; (b) second pregnancy — maternal anti-Rh antibodies crossing the placenta and destroying foetal RBCs; (c) prevention — injection of anti-Rh antibody into the mother.
10.3 Common Human Diseases
A disease is a condition of disturbed or deranged functioning of one or more organs or organ systems of the body, caused by infections, a defective diet, or heredity. Notice what this definition does not say: it does not say that a disease must be caught from someone. Anything that pushes an organ system out of its normal working range is a disease.
How Diseases Are Classified
All human diseases can be broadly categorised into congenital diseases and acquired diseases. The whole classification is set out in FC 10.6, and it is worth keeping this hierarchy in mind, because every disease in this section fits somewhere in it.
Flowchart
FC 10.6 – Classification of human diseases: Human diseases → Congenital diseases (present from birth; genetic abnormality or metabolic disorder) and Acquired diseases (develop after birth) → Acquired diseases branch into Communicable/Infectious diseases (e.g. malaria, typhoid, AIDS) and Non-communicable/Non-infectious diseases (e.g. cancer, deficiency diseases)
Congenital diseases are present from birth. They may be caused by a genetic abnormality or by a metabolic disorder. They may be permanent, and were practically incurable in the past. However, modern research has helped to cure some inborn diseases through gene therapy, enzyme replacement therapy, and similar approaches.
Acquired diseases develop after birth. They can be subdivided into (a) communicable or infectious diseases, and (b) non-communicable or non-infectious diseases.
The diseases which are transmitted from an infected person to another healthy person, either directly or indirectly, are known as communicable or infectious diseases. Malaria and the other transmissible diseases studied in this chapter are examples of this type.
The diseases that cannot be transmitted from an infected person to a healthy one, either directly or indirectly, are known as non-communicable or non-infectious diseases. Cancer and deficiency diseases are examples of this type.
Pathogens, Parasites and Vectors
Communicable diseases are caused by pathogens such as viruses, bacteria, fungi, helminth worms, and so on. All disease-causing organisms are called pathogens.
Many pathogens do not reach us on their own. They use another organism — the vector — to carry them to us. These vectors are actually parasites that we regularly come across.
A parasite is an organism that lives in or on the body of another organism and derives its nutrition from that host organism. Parasites are of two categories: 1. Ectoparasite — lives on the outside of the host’s body, e.g. bedbug. 2. Endoparasite — lives inside the host’s body, e.g. Plasmodium.
Malaria
Malaria is a vector-borne infectious disease caused by a protist, Plasmodium.
There are four species of Plasmodium: P. vivax, P. ovale, P. malariae and P. falciparum. Only P. falciparum causes serious illness, while the others are rarely fatal. Based on the species involved, there are 4 types of malaria — and, as Table 10.4 shows, each species has its own incubation period and its own rhythm of fever.
Table 10.4: Different species of Plasmodium
| Species of Plasmodium | Incubation period | Pattern of high fever |
|---|---|---|
| P. vivax | 14 days | High fever after 48 hr interval |
| P. malariae | 28 days | High fever after 72 hr interval |
| P. ovale | 14 days | High fever after 48 hr interval |
| P. falciparum | 12 days | High fever at irregular intervals, between 36–48 hrs |
Signs and symptoms of malaria
Symptoms of malaria begin to appear about 7 to 15 days after the bite of an infective mosquito.
- The initial symptoms are fever, headache and chills, which may be difficult to recognise as malaria.
- The classical symptom of malaria is the cyclic occurrence of high fever followed by sweating and sudden shivering. Such an entire episode lasts for four to six hours and recurs every two days or three days.
- Vomiting and convulsions.
- Arthralgia (joint pain), and anaemia due to the rupturing of RBCs.
- Haemoglobinuria (haemoglobin appearing in the urine), and hepatomegaly (liver enlargement).
- Retinal damage (eye).
- Cerebral malaria (brain infection).
Notice how several of these symptoms follow directly from one event — the bursting of infected red blood cells. When RBCs rupture in large numbers, haemoglobin is released into the blood and spills into the urine (haemoglobinuria), the count of red cells falls (anaemia), and toxic products released at the same moment trigger the chill-and-fever episode.
Mode of transmission
Plasmodium is transmitted from one person to another through an insect vector — the female Anopheles mosquito. The full life cycle, in both hosts, is shown in Fig. 10.5.
Diagram
Fig. 10.5 – Stages in the life cycle of Plasmodium in mosquito and human; label on the mosquito side: sporozoites (to salivary gland), bursting oocyst, oocyst, mosquito midgut, ookinete, zygote, macrogamete, microgamete; and on the human side: human skin, hepatic cell, hypnozoite (hepatic dormancy), mature schizont, merozoites, erythrocyte, trophozoite, erythrocytic schizont, ruptured erythrocyte, newly infected erythrocyte, gametocyte.
When an infected female Anopheles sucks human blood, it may transfer sporozoites into the human circulation. The sporozoites reproduce asexually through fission (schizogony) in the liver cells or the erythrocytes. The cells formed are now called merozoites. The cells formed within erythrocytes function as gametocytes (gamogony). Besides this, it forms gametocytes within erythrocytes (gamogony).
If the gametocytes are taken up by a female Anopheles, fertilization occurs in its gut. A diploid zygote is formed, which transforms into an oocyst. The oocyst forms a large number of haploid sporozoites through meiosis (sporogony). These sporozoites migrate to the salivary glands and are ready to infect a new human host.
Pause on one detail here: the zygote is diploid (\(2n\)) and the sporozoites formed from it are haploid (\(n\)), because meiosis takes place in between. So the sexual phase of the parasite’s life is completed in the mosquito, not in us — which is why the mosquito, and not the human being, is the definitive host of Plasmodium.
Flowchart
FC 10.7 – Life cycle of Plasmodium: infected female Anopheles bites human → sporozoites enter human blood → liver cells → schizogony (asexual fission) → merozoites → enter erythrocytes → schizogony continues → erythrocytes rupture (fever) → some merozoites form gametocytes → mosquito bites infected human and takes up gametocytes → fertilization in mosquito gut → diploid zygote → oocyst → meiosis (sporogony) → haploid sporozoites → migrate to salivary glands → back to a new human host
Diagnosis and treatment
Malaria can be diagnosed by the microscopic study of a blood smear — the parasite is looked for directly inside the red blood cells. Besides this, other rapid diagnostic tests based on nucleic acid amplification techniques are also used.
Treatment of malaria includes Artemisinin based combination therapies (ACTs). WHO has recommended 5 different ACTs, which include various combinations of artesunate, sulfadoxine, pyrimethamine, and so on. In addition, quinine is also used.
Prevention and control
- Prevention of mosquito bites by using mosquito nets and insect repellents.
- Spraying insecticides, and draining stagnant water where mosquitoes lay their eggs.
- Mosquito larvae can be controlled by using Gambusia, a freshwater fish (biocontrol).
Each of these measures attacks a different point of the life cycle you have just traced: the net blocks the bite, the insecticide kills the adult vector, and Gambusia eats the larvae before they can ever become adults. Break the cycle anywhere, and the disease cannot continue.
Amoebiasis
Amoebiasis is also known as amoebic dysentery. It is a common infection of the human gastro-intestinal tract, which affects 15 % of the population of India.
It is caused by a protist parasite, Entamoeba histolytica. Its life cycle, including the cyst stages by which it survives outside the body, is shown in Fig. 10.6.
Diagram
Fig. 10.6 – Life cycle of Entamoeba histolytica; label trophozoite (with ectoplasm, endoplasm, pseudopodium, nucleus, endosome, food vacuoles, ingested R.B.C.), binary division, precystic form, cyst with chromatoid bodies, binucleate cyst, quadrinucleate cyst (with glycogen vacuoles, nucleus, endosome, chromatoidal body), excystment, cyst wall, metacystic amoeba, division, amoebulae, asexual reproduction.
Signs and symptoms
- Diarrhoea, flatulence, stool with mucus, and abdominal pain (cramps) are common.
- Passing of blood with the stool is common in severe cases.
- Hepatomegaly occurs if the parasite enters the liver. The liver develops an amoebic liver abscess, accompanied by fever and pain in the right abdomen.
Mode of transmission
- Faeco-oral route.
- Eating with dirty hands.
- Contaminated food and water.
The faeco-oral route is exactly what it sounds like: cysts passed out in the faeces of an infected person reach another person’s mouth through unwashed hands, contaminated water, or unwashed food. This single fact explains every one of the preventive measures below.
Diagnosis and treatment
Diagnosis of amoebiasis is made through the microscopic examination of a stool sample.
Amoebiasis is treated by the use of Metronidazole and Tinidazole, which can destroy E. histolytica in the digestive tract as well as in other tissues.
Prevention and control
Wash hands with hot water and soap after using the toilet and after changing a baby’s diaper.
Drink boiled water. Otherwise, water must be chlorinated and filtered. Avoid eating unhygienic food. Vegetables must be properly washed and cooked. Proper sanitary facilities, including sewage disposal, help in prevention.
Ascariasis
Ascariasis is an infectious disease of the human intestinal tract, caused by the roundworm Ascaris lumbricoides. Ascaris lumbricoides is an endoparasitic roundworm, or nematode.
Signs and symptoms
- Gastro-intestinal discomfort accompanied by vomiting and fever.
- Presence of live worms in the faecal matter.
- Pulmonary disorders occur in some patients — pneumonitis (inflammation in the alveolar wall).
- Loss of appetite and weight loss.
- Eosinophilia (the number of eosinophils is increased).
The pulmonary symptoms may seem strange in a disease of the intestine, until you follow the worm’s journey through the body (Fig. 10.7): the larvae do not stay in the gut, but travel through the blood, heart and lungs before returning to the intestine. Passing through the lungs is what inflames the alveolar wall. Eosinophilia is also a clue worth understanding — eosinophils are the white blood cells that rise particularly in worm infestations, so a raised eosinophil count is a hint to the doctor that a helminth may be involved.
Diagram
Fig. 10.7 – Life cycle of Ascaris lumbricoides; label contaminated food → swallowing by man → intestine → blood → heart → lungs → trachea → pharynx → oesophagus → intestine → adult worms in intestine → fertilized eggs in faeces → soil → infective larva develops within the eggs → contaminated food.
Mode of transmission
Food and drinks contaminated with the eggs of these worms are the main mode of transmission. The eggs hatch inside the intestine of the new host. The larvae pass through various organs and settle as adults in the digestive system. The whole route is set out in FC 10.8.
Flowchart
FC 10.8 – Transmission and migration of Ascaris: fertilized eggs passed in faeces → soil → infective larva develops within the egg → contaminated food or water swallowed by man → eggs hatch in intestine → larvae enter blood → heart → lungs → trachea → pharynx → oesophagus → back to intestine → adult worms in intestine → eggs in faeces (cycle repeats)
Diagnosis and treatment
Diagnosis can be done by the microscopic examination of the stool.
Anti-helminthic drugs like Piperazine, Mebendazole, Levamisole and Pyrantel are effective against Ascaris lumbricoides.
Prevention and control
Avoiding defaecation in open spaces prevents the spread of Ascaris. Personal hygienic habits, such as washing hands with water and soap after using the toilet, are also important. Washing vegetables thoroughly before cooking, and avoiding raw vegetables, is important for the prevention of ascariasis.
Filariasis / Elephantiasis
Filariasis is caused by thread-like worms — nematodes. These nematode parasites are transported from person to person via a mosquito bite.
Filariasis can be divided into 3 subtypes: 1. Lymphatic Filariasis 2. Subcutaneous Filariasis (e.g. Loa loa, Mansonella spp.) 3. Serous (abdominal) cavity Filariasis (e.g. Mansonella spp.)
Lymphatic Filariasis (Elephantiasis) is caused by the worms Wuchereria bancrofti, Brugia malayi and Brugia timori.
Signs and symptoms
- Edema with thickening of the skin and the underlying tissue.
- Wuchereria bancrofti affects the legs, arms, breasts, scrotum, and so on.
- In lymphatic filariasis, the worms infect the lymphatic system and cause enlargement of the lymph vessels and nodes. This is elephantiasis — the limbs are swollen like the legs of an elephant.
- Lymphedema, i.e. the accumulation of lymph fluid in the tissue, causing swelling.
- Hydrocele, i.e. the testes are enlarged due to the accumulation of lymphatic fluid in the testis.
The disfiguring swelling has a simple mechanical explanation. The lymphatic vessels normally drain excess tissue fluid back into the blood. When adult worms block and inflame these vessels, that drainage fails; fluid keeps arriving but cannot leave, and the limb swells enormously. The disease does not “grow” the limb — it floods it.
Mode of transmission
Wuchereria bancrofti is transmitted to the human body by the female Culex mosquito. The stages in the mosquito and in the human being are shown in Fig. 10.8.
Diagram
Fig. 10.8 – Mode of transmission of Filariasis (Wuchereria bancrofti); label the numbered stages: (1) mosquito takes a blood meal and L3 larvae enter the skin — infective stage, (2) adults in lymphatics, (3) adults produce sheathed microfilariae that migrate into lymph and blood channels — diagnostic stage, (4) mosquito takes a blood meal and ingests microfilariae, (5) microfilariae penetrate the mosquito’s midgut and migrate to the thoracic muscles, (6) L1 larvae, (7) L3 larvae after two moultings, (8) migration to the head and the mosquito’s proboscis. Mark “Human stages” and “Mosquito stages”.
The larvae escape from the mosquito’s body and arrive on the human skin. They penetrate the skin, undergo two moultings before they become adults, and settle in the lymphatic system. The incubation period can be as long as 8–16 months — one of the longest you will meet in this chapter, which is why the swelling appears long after the bite that caused it.
Flowchart
FC 10.9 – Life cycle of Wuchereria bancrofti: female Culex bites human → L3 larvae enter through the skin → larvae reach the lymphatic system → two moultings → adult worms in lymph vessels → adults produce sheathed microfilariae → microfilariae circulate in lymph and blood → another Culex takes a blood meal and ingests microfilariae → microfilariae penetrate the mosquito’s midgut → migrate to thoracic muscles → L1 larvae → two moultings → L3 larvae → migrate to the mosquito’s proboscis → back to a new human host
Diagnosis and treatment
The use of diethylcarbamazine citrate twice a day for three weeks, and thereafter for five days every six months, is effective against filarial worms.
Prevention and control
Avoid mosquito bites by using mosquito nets and insect repellents. Eradication of mosquitoes is essential for the control of filariasis.
Typhoid
Typhoid is an acute infection of the intestine. It is caused by Salmonella typhi, a Gram -ve bacterium found in the intestinal lumen of an infected person.
Its pathogenicity is due to the “O” antigen, a lipopolysaccharide (LPS) present on the surface coat. The flagella contain the “H” antigen. The main antigens on the bacterium are shown in Fig. 10.9.
Diagram
Fig. 10.9 – Salmonella typhi; label the capsule (K antigen, or Vi in Salmonella), the somatic O antigen (cell wall antigen), and the flagella (H antigen).
These names are worth remembering, because they connect directly back to Section 10.2: the O and H antigens are exactly the epitopes against which the patient’s body makes antibodies — and the diagnostic test for typhoid works by looking for those antibodies.
Signs and symptoms
- Prolonged fever, as high as \(104\,^{\circ}\text{F}\).
- General nausea, fatigue, headache.
- Abdominal pain, constipation or diarrhoea.
- Rose-coloured rash on the skin.
- White coat on the tongue, cough.
- Anorexia (loss of appetite).
- If not treated — breathlessness, irregular heartbeats, haemorrhage.
Mode of transmission
- It is a food and water borne disease.
- Insects like houseflies and cockroaches, feeding on faecal matter, may transfer the bacteria to food material.
- Poor hygiene habits and poor sanitation conditions are responsible for the spread of typhoid.
Diagnosis and treatment
The Widal test is used for the diagnosis of typhoid. Treatment of typhoid involves the surgical removal of the gall bladder in severe cases. Antibiotics like Chloromycetin are a helpful treatment.
For the prevention of typhoid, WHO recommends two vaccines: an oral one (Ty21a vaccine) and an injectable one (Typhoid polysaccharide vaccine), sold as typhim vi and typherix.
Pneumonia
Pneumonia is an inflammatory condition of the lungs, or of the alveoli of the lungs. It is caused by a variety of pathogens — which is an important point in itself, because it means “pneumonia” names a condition of the lung, not a single germ.
The causes may be: - Viruses — influenza virus, adenovirus, para influenza, and Respiratory Syncytial Virus (RSV); - Bacteria — such as Streptococcus pneumoniae; - Fungal pathogens — e.g. Pneumocystis jirovecii and Pneumocystis carinii.
Pneumonia can also be caused by chemical burns or physical injury to the lungs. Some of the infectious agents are shown in Fig. 10.10.
Diagram
Fig. 10.10 – Pneumonia: infectious agents; label Adenovirus, Legionella pneumophila, Streptococcus pneumoniae, and Aspergillus (mould).
Signs and symptoms
- Cough that produces yellow or greenish sputum or phlegm.
- High fever.
- Shortness of breath (dyspnea).
- Chest pain during a deep breath or during coughing.
- Loss of appetite, fatigue, headaches, vomiting, joint pains and muscle aches.
The breathlessness follows directly from the site of the damage. The alveoli are the thin-walled sacs across which oxygen passes into the blood; when they become inflamed and fill with fluid and pus, the gas exchange surface is effectively lost, and the patient must breathe harder for less oxygen.
Mode of transmission
Pneumonia mostly spreads by direct person-to-person contact. It can also spread via droplets released by an infected person, or even by using shared clothes and utensils.
Diagnosis and treatment
The course of treatment depends upon the pathogen leading to the disease — which is why identifying the cause matters so much here. For bacterial pneumonia, antibiotics like Benzyl penicillin, Ampicillin and Chloramphenicol are effective. (Antibiotics, of course, act on bacteria and are of no use against a virus.)
Prevention and control
- Vaccination is an important preventive measure in both children and adults.
- Vaccines against Haemophilus influenzae and Streptococcus pneumoniae in the first year of life help greatly to reduce the chances of causing pneumonia.
Common Cold
The common cold is a viral infectious disease of the upper respiratory region. It is also known as nasopharyngitis, acute viral rhinopharyngitis, acute coryza, or simply a cold.
It is caused by a group of viruses known as Rhinoviruses and Coronaviruses.
Signs and symptoms
- Cough, sore throat, running nose and fever.
- Nasal congestion, sneezing.
- Conjunctivitis (red eyes).
- Muscle rashes, fatigue, headache, shivering and loss of appetite.
Prevention and control
- Staying away from a person suffering from a common cold.
- Washing hands with soap and water.
- Use of a handkerchief to cover the nose and mouth during coughing and sneezing.
- Alcohol-based hand sanitizer can also be used.
Ring Worm (Dermatophytosis)
Ring worm is a fungal infection of the skin. Despite its name, no worm is involved at all — the name comes only from the ring-shaped lesion it produces.
It is caused by many fungal species belonging to the genera Trichophyton and Microsporum. These fungi feed on keratin, the tough structural protein found in skin, hair and nails. This single fact explains where the disease strikes: the fungus grows exactly where its food is.
Signs and symptoms
- Infected skin shows an enlarged, red ring, caused by the ringworm.
- Appearance of dry, scaly lesions on various parts of the body. These red patches cause intense itching.
- Infection of the nails is termed onychomycosis, in which the nails become thick, discoloured and disfigured.
- Athlete’s foot is the fungal infection that usually begins between the toes.
Diagram
Fig. 10.11 – Ring worm; label the fungus living on the dead tissue of the skin, the microscopic appearance of ringworm with fungal hyphae, and the ringworm lesion on the arm.
Mode of transmission
Ringworm spreads by the sharing of clothes and combs of an infected person. Close contact with an infected person is another mode of infection.
Diagnosis and treatment
Diagnosis is by physical examination, and treatment uses drugs like nystatin, fluconazole, itraconazole, and so on.
Prevention and control
Avoid close contact, and avoid sharing clothes and sports equipment. Washing clothes in hot water with fungicidal soap helps to destroy the fungal pathogen. Athlete’s foot is common in damp, enclosed footwear precisely because fungi grow best in warmth and moisture — keeping the skin dry is therefore itself a preventive measure.
Dengue
Dengue fever is a painful, debilitating vector-borne disease, caused by any one of four closely related dengue viruses.
The dengue virus is transmitted through the bite of the female Aedes mosquito. The mosquito takes up the dengue virus when it sucks the blood of a person suffering from dengue. Dengue cannot spread directly from one person to another person — it always needs the mosquito in between.
Cancer
Abnormal, uncontrolled and purposeless division of cells may lead to the formation of a mass of undifferentiated cells, i.e. a tumor. When a tumor is malignant, it is described as cancer, and it has the ability to invade other tissues.
Every word in that description is doing work. Uncontrolled, because the normal brakes on cell division have failed. Purposeless, because the new cells serve no function for the body. Undifferentiated, because they never mature into a proper tissue type.
Cancer harms the body when cancerous cells divide uncontrollably to form new lumps or masses of tissue called neoplasm (except in the case of leukemia, where the abnormal cells circulate in the blood rather than forming a lump). Tumors can grow and interfere with the normal functioning of various organs. They also release secretions which alter body functions.
It is one of the main killer diseases nowadays. Physicians and researchers who specialise in the study, diagnosis, treatment and prevention of cancer are called oncologists.
Tumors may develop anywhere in the body. However, all tumors are not cancerous. There are two types of tumors: benign or non-malignant, and cancerous or malignant. The difference is visible even under the microscope, as Fig. 10.12 shows.
Diagram
Fig. 10.12 – Benign and malignant tumor; in the benign panel label normal tissue cells, connective tissue capsule and abnormal cells enclosed within it; in the malignant panel label normal tissue cells and cancer cells invading between them without a capsule.
1. Benign or non-malignant tumor
A benign tumor grows slowly. It may attain quite a large size, but it remains restricted to the site of its origin (localized) and does not spread to other parts of the body.
This does not necessarily mean that benign tumors are not troublesome. Some benign tumors are harmful and even fatal — for example, a brain tumor. (A brain tumor may cause death because the brain is squeezed against the hard skull; the tumor need not spread anywhere to kill.) Moreover, benign tumors may sometimes become malignant, e.g. adenoma and fibroid.
2. Malignant tumor or cancer
The growth rate of this tumor is rapid, and the mortality rate is comparatively higher than that of a benign tumor. Rapid growth of the tumor causes overcrowding and disruption of the normal cells. The cancerous cells compete with the normal cells for nutrients and finally kill them.
These cells spread from one organ to another via the blood or lymph and form new tumors, called secondary tumors. This migratory process is called metastasis.
Metastasis is the single feature that makes cancer so dangerous. A localized lump can be cut out; cells that have already scattered through the bloodstream cannot.
a. Types of cancer
There are five main types of cancers, according to the type of tissue affected. Cancers are named according to the tissue from which they arise — so if you know the tissue, you can usually name the cancer.
i. Carcinoma: Cancer that arises from the epithelial tissue covering or lining the body organs is known as carcinoma. It includes breast cancer, lung cancer, cancer of the stomach, skin cancer, and so on.
ii. Sarcoma: Cancer that arises from connective tissue is called sarcoma. It includes bone tumors (osteosarcoma), muscle tumors (myosarcoma), cancer of cartilage (chondrosarcoma) and cancer of adipose tissue (liposarcoma).
iii. Lymphoma: Cancer that arises from lymphatic tissue is called lymphoma. It occurs in the lymphatic nodes, spleen and tissues of the immune system.
iv. Leukemia: It is a type of blood cancer in which there is excessive formation of white blood cells (WBCs) or leucocytes in the bone marrow. People suffering from leukemia have a very high leucocyte count. The blood contains millions of abnormal, immature WBCs or leucocytes that are incapable of fighting infections. There are various types of leukemia, such as monocytic leukemia and lymphoblastic leukemia.
Note the cruel irony in leukemia: the patient has more white blood cells than a healthy person, yet is more vulnerable to infection — because those cells are immature and cannot do the immune work you studied in Section 10.1. Quantity is not the same as function.
v. Adenocarcinoma: Adenocarcinoma arises in the thyroid, pituitary, adrenal and other glandular tissues.
b. Causes of cancer
Although it is still not very clear exactly how cancer is caused, several factors are now known to be cancer-causing, i.e. carcinogenic. These factors are as follows.
i. Chemicals: Several chemicals are known to induce cancer. These include nicotine, caffeine, and the products of combustion of coal and oil. Several polycyclic hydrocarbons, some sex hormones and steroids, if given or secreted in large amounts, may cause cancer. Breast cancer seems to have a hormonal relationship — it is more commonly observed in women who avoid breast feeding.
ii. Radiation: X-rays, gamma rays, cosmic rays, ultra-violet rays, and so on, are carcinogenic. The incidence of skin cancer is higher in people working in very sunny areas, due to the UV radiation in sunlight.
iii. Viruses: Viruses causing cancer have genes called viral oncogenes (v-onc genes). These viruses are also called oncogenic viruses, e.g. EBV (Epstein-Barr virus) and HPV (Human Papilloma Virus).
iv. Oncogenes: Several genes called cellular oncogenes (c-onc genes), or proto-oncogenes, have been identified in normal cells. When activated under certain conditions, these could lead to the oncogenic transformation of cells.
Read that last point carefully, because it is the heart of the modern understanding of cancer: the genes that turn a cell cancerous are already present in our own normal cells. In a normal cell they are proto-oncogenes, and they do the ordinary job of controlling cell division. Carcinogens do not add new genes — they activate or damage the ones that are already there.
v. Addiction: Different types of addictions, such as smoking and the chewing of tobacco, lead to cancer of the mouth, lips and lungs. Alcohol consumption may result in cancer of the oesophagus, stomach, intestine and liver. Drugs also cause cancer, e.g. marijuana and anabolic steroids.
Flowchart
FC 10.10 – How cancer develops: carcinogen (chemical, radiation, oncogenic virus, tobacco/alcohol) → damage to or activation of proto-oncogenes (c-onc genes) in a normal cell → loss of control over cell division → uncontrolled, purposeless division → mass of undifferentiated cells (tumor) → if benign: remains localized; if malignant: invades surrounding tissue → cells enter blood or lymph → metastasis → secondary tumors in other organs
Table 10.13: Carcinogens and organ affected
| Carcinogen | Organ affected | |
|---|---|---|
| 1. | Soot | Skin, lungs |
| 2. | Coal tar (3,4 benzopyrene) | Skin, lungs |
| 3. | Cigarette smoke (N-nitrosodimethylene) | Lungs |
| 4. | Cadmium oxide | Prostate gland |
| 5. | Aflatoxin (a metabolite of Aspergillus flavus, a mould) | Liver |
| 6. | 2-naphthylamine and 4-aminobiphenyl | Urinary bladder |
| 7. | Mustard gas | Lungs |
| 8. | Nickel and chromium compounds | Lungs |
| 9. | Asbestos | Lungs |
| 10. | Diethylstilbestrol (DES) | Vagina |
| 11. | Vinylchloride (VC) | Liver |
c. Treatment of cancer
Cancer treatment consists of a combination of a number of therapies, which are as follows:
i. Chemotherapy: Chemotherapy comprises the administration of certain anticancer drugs. The anticancer drugs check cell division by inhibiting DNA synthesis, or are more toxic to cancerous cells than to normal cells. Chemotherapy may lead to hair loss or anaemia, but both get corrected after the treatment is stopped. (The side effects follow from the drug’s mechanism: it hits rapidly dividing cells, and hair-root cells and blood-forming cells in the bone marrow also divide rapidly.)
ii. Radiotherapy: It is used in addition to chemotherapy. In radiotherapy, the basic principle is to bombard the cancerous tissue or cells with rays from radioactive materials. For treatment, the cancer tissue or cells are exposed to radiations from radioactive materials such as cobalt, iridium and iodine. X-rays, gamma rays and charged particles are used to destroy the cancerous tissue or cells, but to cause minimum damage to the surrounding normal tissue or cells.
iii. Surgery: In surgery, the entire cancerous tissue or cells are removed surgically. It has limited utility. In certain cases, such as breast tumor or uterine tumor, surgery is most effective, but other treatments are also given to kill any cancerous cell that may have escaped in surgery.
iv. Immunotherapy: Tumor cells have been shown to avoid detection and destruction by the immune system. Therefore, patients are given substances called biological response modifiers, such as \(\alpha\)-interferon, which activate their immune system and help in destroying the tumor. This is the immune system of Section 10.1 being deliberately reinforced — the body’s own defence, turned back onto the cancer.
v. Supportive therapy: Supportive therapy is used to treat the symptoms of cancer and the side effects of cancer treatments. The objective of this therapy is to improve the quality of life of the cancer patient. This therapy varies depending upon the condition of the individual patient.
AIDS
AIDS — the acquired immuno deficiency syndrome — is a usually fatal illness caused by a retrovirus (ss RNA) known as the human immuno deficiency virus (HIV).
HIV weakens the body’s immune system, leaving the victim vulnerable to life-threatening opportunistic infections, neurological disorders and unusual malignancies. The word “opportunistic” is important: these are infections by organisms that a healthy immune system would brush aside without difficulty, and which get their opportunity only because the defence has collapsed. In this sense, HIV rarely kills directly — it removes the defence, and something else does the killing.
AIDS can be called a modern pandemic (worldwide), affecting both industrialised and developing countries.
AIDS was first noticed in the USA in 1981. In India, the first confirmed case of AIDS was in April 1986, from Tamil Nadu.
Structure of HIV
HIV is 100 to 140 nm in diameter, and it is spherical. The virus particle shows two centrally located ss RNA molecules, along with reverse transcriptase enzymes.
It is covered by two layers of proteins: the outer layer is of matrix protein (p17), while the inner layer is capsid protein (p24). Over the matrix protein layers there is an additional layer of lipids, impregnated with the glycoproteins GP120 and GP 41. All these parts are labelled in Fig. 10.14.
Diagram
Fig. 10.14 – Structure of HIV; label Gp120 and Gp 41 spikes, lipid coat, matrix proteins (outer), capsid proteins (inner), the two single-stranded RNA molecules, and reverse transcriptase.
The virus replicates in actively dividing \(T_4\) lymphocytes, and can remain in a latent state or stage in the lymphoid cells. The virus has the unique ability to destroy human \(T_4\) lymphocytes.
Now connect this to what you already know. The \(T_4\) lymphocytes are the helper T-cells — the coordinators that stimulate B-lymphocytes and macrophages. HIV therefore does not merely attack the immune system; it attacks the commander of the immune system. Once the helper T-cells are destroyed, the antibody-mediated and cell-mediated responses both lose their signal to act, and the whole defence unravels. That single targeting choice explains the entire disease.
HIV is found in the greatest concentration in blood, semen and cerebrospinal fluid (CSF), and to a lesser extent in tears, milk, urine, saliva, and cervical and vaginal secretions.
Transmission of HIV
The virus can be transmitted through:
- Unsafe sexual contact: including oral, vaginal and anal sex.
- Blood: via blood transfusions or needle sharing.
- From mother to child (transplacental): a pregnant woman can transmit the virus to her foetus through their shared blood circulation; or a nursing mother can transmit it to her baby through her breast milk.
Other methods of spreading the virus are rare, and include accidental needle injury, artificial insemination with infected donated semen, and transplantation with infected organs.
The AIDS virus has been found in urine, tears, saliva, breast milk and vaginal secretions, but it seems not to be transmitted by these fluids unless it gets into injuries.
Clinical manifestations
The clinical manifestations (symptoms) of AIDS have been classified into four broad categories, which follow one another as the disease advances (FC 10.11).
i. Initial infection with the virus, and the formation of antibodies, usually 2–8 weeks after the initial infection.
ii. Asymptomatic carrier state, in which no signs of disease are seen. The incubation period ranges from 6 months to 10 years. This long silent stage is why HIV spreads so effectively: a person can feel entirely well, be unaware of the infection, and still transmit the virus for years.
iii. AIDS related complex (ARC), with one or more of the following clinical signs: recurrent fever for longer than one month, fatigue, unexplained diarrhoea, night sweats, shortness of breath, and loss of more than 10 per cent of body weight.
iv. AIDS is the end stage of HIV infection. It is characterised by life-threatening opportunistic infections such as pneumonia, tuberculosis, kaposi sarcoma, and others.
Flowchart
FC 10.11 – Progression of HIV infection: HIV enters the body → initial infection, antibodies formed 2–8 weeks later → asymptomatic carrier state (no signs; 6 months to 10 years) → AIDS related complex (ARC): recurrent fever, fatigue, diarrhoea, night sweats, weight loss → AIDS (end stage): opportunistic infections such as pneumonia, tuberculosis, kaposi sarcoma
Preventive measures
AIDS has no cure, hence prevention is the best choice. The following steps help in preventing this dreadful disease:
- People, particularly those in high-risk groups, should be educated about HIV transmission.
- Disposable needles and syringes should be used, and disposed of properly and immediately.
- Sexual habits should be changed immediately.
- High-risk groups should refrain from donating blood.
- Toothbrushes, razors, and other articles that can become contaminated with blood should not be shared.
- Before receiving blood, ensure that it has been screened for HIV infection.
- Routine screening must be done for —
- blood donors;
- organ donors (kidney, liver, lung, cornea);
- donors of semen and growth hormone;
- patients undergoing haemodialysis, and females in high-risk groups who are pregnant or contemplating pregnancy.
Laboratory diagnosis
Diagnosis is done in two steps, and the reason for the two steps is worth understanding. At first a test is used to detect the HIV antibodies, and then a second, confirmatory test is used to weed out any false positive results.
The first test is ELISA (Enzyme-Linked Immunosorbent Assay). The confirmatory test, usually a Western Blot, is a highly specific test. It is based on detecting specific antibodies to the viral core protein and envelope glycoprotein.
The logic is that of screening: the first test is sensitive, so that no true case is missed, but for that very reason it will occasionally flag someone who is not infected. The second test is highly specific, and its job is to confirm. No one should ever be declared HIV positive on the basis of the screening test alone.
Treatment of AIDS
Although AIDS has no cure, certain medicines called antiretroviral drugs can help in reducing the viral load and prolonging the life of an HIV patient. Examples of these drugs, used in antiretroviral therapy (ART), are TDF (tenofovir), EFV (efavirenz), lamivudine (3TC), and others.
Looking Back at the Battle
The advancements made in the biological sciences have helped us to deal effectively with many infectious diseases.
The use of vaccines and immunization programmes has enabled us to eradicate completely such dreadful diseases as small pox. A large number of other infectious diseases — polio, diphtheria, pneumonia and tetanus — have been controlled to a large extent by the use of vaccines. Biotechnology is on the verge of making available newer and safer vaccines. The discovery of antibiotics and various drugs has also enabled us to treat infectious diseases such as tuberculosis effectively.
Look back over this section and notice the single thread running through it. For every disease, we asked the same four questions: what is the pathogen, how does it reach us, what does it do inside us, and where can the chain be broken? That is the reasoning a doctor and a public health worker use — and it is what NEET and board questions on this section really test, usually as match-the-following (disease → pathogen → vector) or as “what happens if” reasoning about a stage of a life cycle.
10.4 Adolescence
Adolescence is the period that begins with the appearance of secondary sexual characters and terminates with the cessation of somatic (body) growth.
It can also be regarded as a transitional stage of the physical and mental development of a child, occurring between puberty and legal adulthood, between 10 to 19 years of age — a stage in which the individual is no longer a child, but not yet an adult.
Adolescence is, in fact, a phase rather than a fixed time period in life. Two people of the same age may be at quite different points in it. It is a phase of development on many fronts at once: sexual and reproductive maturity, mental development, the formation of an adult identity, and the transition from socio-economic and emotional dependence to relative independence.
Stages of Adolescence
Adolescents are defined as individuals of the 10 to 19 year age group. The Government of India, in its National Youth Policy, defines adolescents as 13–19 years.
Adolescence is divided into three stages (periods): the early stage, the middle stage and the late stage. These are summarised in FC 10.12.
Flowchart
FC 10.12 – Stages of adolescence: Early period (10–14 years) → secondary sexual characters begin to appear, growth reaches its peak, concrete thinking, self exploration → Middle period (15–17 years) → secondary sexual characters almost complete, physical growth slows, about 95 % of adult stature attained, abstract thinking, strong peer group → Late period (18–19 years) → total physical maturity, established abstract thinking, intellectual and functional identity, stable individual relationships
i. Early period (10 to 14 years)
The changes in this stage include the beginning of the appearance of secondary sexual characters, and growth reaching its peak — this is the phase of the fastest physical growth. Thinking at this stage is still largely concrete, that is, tied to real, visible, immediate things rather than to abstract ideas.
Other features of the early period are the defining of the boundaries of dependence and independence, self exploration, the development of a body image, the development of intense friendships, and the seeking of ways to counter instability, along with self-evaluation.
ii. Middle period (15 to 17 years)
This stage is characterised by the almost complete development of secondary sexual characters. Physical growth slows down, and approximately 95 % of the adult stature is attained.
Thinking becomes more abstract — the adolescent can now reason about possibilities, principles and consequences, not just about what is in front of them. However, under stressful conditions the thinking may fall back to the concrete level. There is a capability for long-range thinking, that is, for planning ahead.
The other features are a re-establishing of body image, a sense of leadership and of being all-powerful, preoccupation with romantic fantasy and attraction towards the opposite sex, and the establishing of a peer group that helps in defining a behavioural code.
iii. Late period (18 to 19 years)
This stage is characterised by the establishment of total physical maturity, established abstract thinking, and an intellectual and functional identity.
The peer group now recedes in favour of individual relationships. Relationships become stable, and there is a change from childhood to adulthood relationships — the young person begins to relate to others as an adult among adults.
Physical Changes of Adolescence
Growth spurt occurs in both boys and girls — a sudden acceleration in height and body size.
In boys, the muscles develop, the skin becomes oily, the shoulders broaden, the voice cracks, and there is development of underarm and chest hair, pubic hair and facial hair, along with enlargement of the penis and testes.
In girls, there is development of the breasts, widening of the hips, development of underarm and pubic hair, and enlargement of the uterus and ovaries. The main changes in both are shown in Fig. 10.20.
Diagram
Fig. 10.20 – Physical changes of adolescence; two panels (boy and girl) with labels — boy: broadening of shoulders, muscle development, oily skin, facial and chest hair, cracking of voice, enlargement of penis and testes; girl: development of breasts, widening of hips, underarm and pubic hair, enlargement of uterus and ovaries.
Sexual development: The sex organs mature and enlarge. There is sexual desire, erection of the penis in boys, sperm production and ejaculation; ovulation and menstruation in girls; and the initiation of sexual behaviour.
All these changes are the outward, visible result of hormones released at puberty. That is why they appear together, in a coordinated sequence, rather than one at a time — and it is also why the timing differs from person to person without anything being wrong.
Mental Health and Adolescence
Many of the emotional and social changes just described have implications for mental health. In fact, most of the mental health issues that people confront as adults begin to appear in adolescence — which is precisely why this stage deserves attention rather than dismissal.
The mental health implications include confusion, irritation, moodiness, frustration, nausea, reduced concentration, hyperactivity and anger, along with effects on lifestyle such as obesity, addictions and accidents, leading to ill health. Mental illness, in fact, often appears in terms of different forms of depression, such as insomnia and loss of energy.
Thus, mental illness (disorders, or unfavourable changes) is associated with psychological or behavioural manifestations. These are broadly classified as either psychoses or neuroses.
Psychoses include delusions, hallucinations, and disturbance in the thinking process. The psychoses lead to Alzheimer’s disease, schizophrenia, depressive psychosis, amnesia (loss of memory), bulimia (extreme over-indulgence in food), anxiety (fear or apprehension), anorexia nervosa (emotional aversion to food), and depression (sadness, inactivity, reduced interest in enjoying life).
Neuroses include schizophrenia, illusions, and hallucination.
Adolescence is thus characterised by a number of cognitive, emotional, behavioural, physical and attitudinal changes. These may lead to positive personality development, which depends upon the relationship with parents and on other conditions — or they may lead to conflicts with others.
In fact, adolescents view their friends and their peer group as more important and more influential than their parents. This is a normal part of forming an identity, but it also carries a risk: it may lead to various kinds of addictions, such as smoking and taking drugs. That risk is the subject of the next two sections.
Treatment
Treatment of such disorders should preferentially be with a non-pharmacological approach — that is, through counselling, therapy and support rather than beginning with medicines — with due respect to the rights of children.
WHO has recommended evidence-based guidelines under the mental health Gap Action Programme (mhGAP), which is designed to make basic mental health care available to people who might otherwise never receive it.
10.5 Addiction
Addiction is a complex condition characterised by the compulsive use of a substance despite its harmful consequences. Read that definition slowly, because the important words are “compulsive” and “despite”.
Addiction is not simply the act of using something; it is the loss of the ability to stop, even after the person clearly knows the harm being done. This is why addiction is treated as a medical condition and not as a mere failure of willpower.
Addiction may involve the use of substances (drugs) such as alcohol, opioids, cocaine, nicotine and others, or behaviours such as gambling. The fact that a behaviour with no chemical involved can become addictive is itself a clue about where addiction actually lives — not in the substance, but in the brain.
What Addiction Does Inside the Brain
There is scientific evidence that addictive behaviours share key neurobiological features. They intensely involve the brain pathways of reward and reinforcement, which affect motivation, and which involve the neurotransmitter dopamine.
The brain’s reward pathway normally exists for a good reason: it releases dopamine when we do something useful for survival — eating when hungry, achieving something, being with people we care for — and the pleasant feeling that results makes us repeat that action. Addictive substances hijack this system. They produce a surge of dopamine that is far larger than anything an ordinary activity produces, and the brain’s reward circuit learns, powerfully, to seek that substance again. The sequence is set out in FC 10.13.
Flowchart
FC 10.13 – The reward pathway in addiction: drug or addictive behaviour → large surge of dopamine in the brain’s reward pathway → intense pleasure/euphoria → reinforcement (the brain marks the act as “worth repeating”) → strong motivation to repeat → repeated use → reward pathway alters, ordinary pleasures feel flat → compulsive use despite harm = addiction
It is important to know that the neurological changes are reversible after the substance use or the behaviour is discontinued. The brain’s reward pathway can recover. This is one of the most hopeful facts in this chapter, and it is the biological reason why de-addiction programmes work — the damage is not a life sentence.
Overall, addiction results in the impairment of the physical, physiological and psychological functions of the body. Notice that all three levels are affected together — the body is damaged, the internal processes are disturbed, and thinking, mood and behaviour change as well.
Causes of Substance Abuse During Adolescence
Adolescence, as you saw in the previous section, is a phase of identity formation, peer influence and emotional instability — and that is exactly why it is the stage at which substance use most often begins. The commonly identified causes are:
- Insufficient parental supervision and monitoring.
- Lack of communication between the child and the parents.
- Poorly defined rules.
- Family conflicts.
- Favourable parental attitudes towards alcohol and drug use.
- Expectations from drug use — that is, the belief that the drug will deliver confidence, relief or belonging.
- Risk-taking behaviour.
Look at this list carefully. Almost every item is about the environment around the adolescent, not about the drug itself. That is a useful thing to notice, because it tells us where prevention has to act.
Methods and Measures to Control Drug Abuse
Always remember: “Prevention is better than cure.” Once the reward pathway has been altered, stopping is far harder than never starting.
Avoid undue pressure. A child should not be forced to perform beyond his or her capacities in studies, sports or other activities. Pressure that a young person cannot handle is one of the situations that pushes them towards escape.
Education and counselling of the child — to face problems and stress, and to accept disappointments and failures as a part of life. Channelize the energy of the child into sports, studies and other constructive activities, so that the need for stimulation and achievement is met in ways that build rather than destroy.
10.6 Drugs Abuse
Surveys and statistics show that the use of drugs and alcohol has been on the rise, especially among the youth. This is a real cause of concern, because it can result in many harmful effects — on the body, on the mind, and on the family and society around the user.
Proper education and guidance would enable young people to safeguard themselves against these dangerous behaviour patterns and to follow a healthy lifestyle. This is the reason a chapter on health includes a section on drugs at all: knowing what a drug does to the body is itself a form of protection.
The drugs which are commonly abused are the opioids, the cannabinoids, and the alkaloids of coca. Each of them comes from a plant, and each of them acts on receptors that already exist in our nervous system. The plant sources are shown in Fig. 10.21.
Diagram
Fig. 10.21 – Plant sources of commonly abused drugs; label (a) Papaver somniferum (poppy) with latex being collected from the unripe capsule → opioids (heroin/smack), (b) Cannabis sativa with inflorescence → cannabinoids (marijuana, hashish, charas, ganja), (c) Erythroxylum coca → cocaine.
a. Opioids
These drugs bind to opioid receptors present in the central nervous system and in the gastro-intestinal tract.
Heroin, otherwise called smack, is chemically di-acetyl morphine. It is extracted from the latex of the poppy plant, Papaver somniferum.
Heroin is a depressant — it slows down the activity of the body. Because opioid receptors are present in the brain stem, which controls breathing, a large dose can slow the breathing so much that it stops altogether. This is the direct reason why an opioid overdose kills.
b. Cannabinoids
Cannabinoids interact with receptors present in the brain. Inhalation and ingestion of these substances affect the cardiovascular system — that is, the heart and blood vessels.
These are obtained from the inflorescences and other parts of Cannabis sativa. Marijuana, hashish, charas and ganja are the different forms of the drugs obtained from this plant.
c. Cocaine
Cocaine is an alkaloid obtained from the coca plant, Erythroxylum coca.
It increases the level of the neurotransmitter dopamine. You already know why that matters: dopamine is the transmitter of the brain’s reward pathway, so raising its level artificially produces an intense but false sense of reward — and it is exactly this that drives the user back to the drug.
Its excessive dosage causes extreme happiness, irritability and paranoia (an unreasonable, persistent feeling of being threatened or watched).
Hallucinogens (Mind-Expanding Drugs)
These are alkaloids that cause day-dreaming. Lysergic acid and cannabis are hallucinogenic substances. Atropa belladonna and Datura spp. also have hallucinogenic properties.
A hallucination is the unreal perception of an unreal object, due to a disorder of the nervous system. In other words, the person genuinely sees or hears something that is not there at all. This is not imagination under the person’s control — it is a malfunction of the sensory processing of the brain, which is why hallucinogens are dangerous rather than merely strange.
Addiction and Dependence
Because of the perceived benefits — the temporary “high”, the momentary relief — drugs are used repeatedly. The most important thing, which one fails to realise, is the inherent addictive nature of alcohol and drugs.
Addiction, as you have seen, is a psychological attachment to certain effects, such as euphoria and a temporary feeling of well-being, associated with drugs and alcohol. These drive people to take them even when they are not needed, or even when their use becomes self-destructive.
With repeated use of drugs, the tolerance level of the receptors present in our body increases. Consequently, the receptors respond only to higher doses of the drug or alcohol, leading to greater intake and to addiction. This is a trap with a mathematical shape to it: the same dose gives less and less effect, so the dose must be raised, which raises tolerance further, which demands a still higher dose.
However, it should be clearly borne in mind that the use of these drugs even once can lead to addiction. In the absence of any guidance or counselling, the person gets addicted and becomes dependent on their use.
Dependence is the tendency of the body to manifest a characteristic and unpleasant withdrawal syndrome if the regular dose of the drug or alcohol is abruptly discontinued. This is characterised by anxiety, trembling, nausea and sweating, which may be relieved when the use is resumed — and that relief is precisely what locks the person in. The cycle is set out in FC 10.14.
Flowchart
FC 10.14 – The cycle of addiction and dependence: first use → euphoria/perceived benefit → repeated use → tolerance of receptors increases → the same dose no longer works → higher dose taken → addiction (compulsive use) → dependence → dose stopped abruptly → withdrawal syndrome (anxiety, trembling, nausea, sweating) → use resumed for relief → back into the cycle
Effects of Drug and Alcohol Abuse
The immediate adverse effects of drug and alcohol abuse are manifested in the form of reckless behaviour, vandalism and violence.
Excessive doses of drugs may lead to coma and death, due to respiratory failure, heart failure, or cerebral haemorrhage. A combination of drugs, or their intake along with alcohol, generally results in overdose and even death — because two depressants taken together suppress breathing and heart action far more than either would alone.
Warning signs
The most common warning signs of drug and alcohol abuse among the youth include: a drop in academic performance; unexplained absence from school or college; lack of interest in personal hygiene; withdrawal and isolation; depression; fatigue; aggressive and rebellious behaviour; deteriorating relationships with family and friends; loss of interest in hobbies; change in sleeping and eating habits; and fluctuations in weight and appetite.
These signs are worth knowing not so that anyone may be judged, but so that help can be offered early — a change in a friend’s behaviour is often the first thing anyone notices, long before any medical test would.
Wider consequences
There may even be some far-reaching implications of drug and alcohol abuse. If an abuser is unable to get money to buy drugs or alcohol, he or she may turn to crime. At times, a drug or alcohol addict becomes the cause of mental and financial distress to his or her entire family and friends.
Those who take drugs intravenously (direct injection into a vein using a needle and syringe) are likely to acquire serious infections like HIV and hepatitis B. The reason connects straight back to what you learnt about AIDS: a shared needle carries blood from one person into the bloodstream of the next, and blood is the fluid in which HIV is present in the greatest concentration.
The use of alcohol during adolescence may also have long-term effects, such as loss of balance, liver cirrhosis and pancreatitis. It could also lead to heavy drinking in adulthood.
Chronic use of drugs and alcohol damages the nervous system and the liver (cirrhosis). The liver is the organ that detoxifies what we consume, so it takes the heaviest chemical load — and in cirrhosis its functioning tissue is progressively replaced by scar tissue, which cannot do the work.
The use of drugs and alcohol during pregnancy adversely affects the foetus, because these substances cross the placenta and reach a developing body that has no capacity to handle them.
Misuse of drugs in sports
Another misuse of drugs is that certain sportspersons use drugs to enhance performance. They misuse narcotic analgesics, anabolic steroids, diuretics and certain hormones, in order to increase muscle strength and bulk, to promote aggressiveness, and to bring about an overall improvement in their performance.
The side-effects of the use of anabolic steroids in females include masculinization (the appearance of male-like features), increased aggressiveness, mood swings, depression, abnormal menstrual cycles, excessive hair growth on the face and body, enlargement of the clitoris, and deepening of the voice.
In males, the side-effects include acne, increased aggressiveness, mood swings, depression, reduction in the size of the testicles, decreased sperm production, kidney and liver dysfunction, breast enlargement, premature baldness, and enlargement of the prostate gland.
These effects may be permanent with prolonged use — which is the point that no advertisement for such substances ever mentions.
Prevention and Control
The age-old adage — “prevention is better than cure” — holds true for all addictions.
It is also true that habits such as smoking, taking drugs, or drinking alcohol are more likely to be taken up at a young age, and most often during adolescence. That is not an accident: as you saw in Section 10.4, this is exactly the stage of peer influence, risk-taking and identity formation.
It is best to identify the situations that push an adolescent towards the use of drugs or alcohol, and to take remedial measures well in time. In this regard, the parents and the teachers have a special responsibility — because they are the people in a position to notice the warning signs early, and to offer help before dependence has set in.
10.7 Summary
Health is not merely the absence of disease. WHO defines it as a state of complete physical, mental and social well-being. It reflects the metabolic and functional efficiency of the body, and it is supported by hygiene, a balanced diet, clean water, exercise, waste disposal and vector control.
The immune system protects us from infectious agents. Its central skill is telling self (the body’s own cells) from non-self (foreign molecules and invading cells). Any foreign substance that stimulates an immune response is an antigen; the protective chemicals made against it are antibodies. Immunology is the study of this system; the concept of immunity began with Edward Jenner and his cowpox vaccine against small pox.
Innate (inborn) immunity is inherited, present from birth, and not affected by prior contact with microbes. It includes: epithelial barriers (skin, salt in drying sweat, sebaceous secretions, nasal hair and mucus, cough reflex, saliva, gastric acidity, flushing action of urine, spermine and zinc in semen, and lysozyme in tears); antimicrobial substances in blood and tissues (the complement system of over 30 serum proteins, and interferons); cellular factors (phagocytes — microphages and macrophages, discovered by Metchnikoff in 1882 — and NK cells); fever; and acute phase proteins (CRP, mannose binding protein, alpha-1-acid glycoprotein, serum amyloid P).
Acquired (adaptive) immunity develops during life and has four features: specificity, diversity, discrimination between self and non-self, and memory. It is of two types — active (the body makes its own antibodies; natural, as after measles, or artificial, as by vaccines; long-lasting) and passive (readymade antibodies are received; natural, through the placenta and colostrum, or artificial, as anti-rabies serum from hyper-immunised horses; short lived).
Lymphocytes arise from stem cells (haemocytoblasts) in the foetal liver and adult bone marrow. Those differentiating in gut-associated bursal lymphoid tissue become B-lymphocytes (antibody-mediated immune system, AMIS); those differentiating in the thymus become T-lymphocytes (cell-mediated immune system, CMIS).
A T-cell clone has four types: helper T-cells (secrete lymphokines), killer/cytotoxic T-cells (secrete perforins), suppressor T-cells, and memory T-cells. Activated B-cells form plasma cells (which secrete antibodies at about 2000 molecules per second) and memory B-cells. Free antibodies act by agglutination, opsonisation and neutralization. Antigen presenting cells engulf and process antigens, display them, and activate helper T-cells.
Vaccination is the administration of an inactivated pathogen or an antigenic preparation to protect against that pathogen. Vaccines may be a protein or sugar from the pathogen, a dead/inactivated pathogen, a toxoid, or a weakened (attenuated) pathogen. Vaccination is a form of primary prevention; it protects the individual and, when coverage is high, the whole society.
An antibody (immunoglobulin) is a Y-shaped glycoprotein of four polypeptide chains — two heavy (H) and two light (L) — joined by disulfide bonds, with a hinge region. Each chain has a variable and a constant region. The variable regions form the antigen-binding site (paratope); most antibodies are bivalent. The epitope (antigenic determinant) of the antigen binds the paratope in a lock-and-key manner to form the antigen-antibody complex. The study of these interactions is serology.
Blood group antigens sit on the surface of RBCs (ABO, Rh, Duffy, Kidd, Lewis, P, MNS, Bombay systems). Karl Landsteiner discovered A, B and O (1900); Decastello and Sturli discovered AB (1902). Group A has antigen A and antibody b; group B has antigen B and antibody a; group AB has both antigens and no antibodies (universal acceptor); group O has no antigen and both antibodies (universal donor).
The Rh factor (D antigen), discovered by Landsteiner and Wiener (1940) on Rhesus monkey RBCs, defines Rh +ve and Rh -ve people. When an Rh -ve mother carries an Rh +ve foetus, foetal RBCs entering her blood at childbirth make her produce anti-Rh antibodies; a later Rh +ve foetus is then attacked, causing erythroblastosis foetalis (HDN). It is prevented by injecting anti-Rh antibody into the mother during all pregnancies carrying an Rh +ve foetus.
A disease is disturbed or deranged functioning of one or more organs or organ systems, caused by infection, defective diet or heredity. Diseases are congenital (present from birth) or acquired (after birth); acquired diseases are communicable/infectious or non-communicable/non-infectious. Disease-causing organisms are pathogens; a vector carries a pathogen to us. Parasites are ectoparasites (e.g. bedbug) or endoparasites (e.g. Plasmodium). The incubation period is the time from invasion by the pathogen to the appearance of clinical signs.
Malaria — caused by Plasmodium (P. vivax, P. ovale, P. malariae, P. falciparum; only P. falciparum causes serious illness); vector: female Anopheles. Sporozoites → schizogony in liver and RBCs → merozoites → gametocytes → fertilization in the mosquito gut → zygote → oocyst → sporogony (meiosis) → sporozoites in salivary glands. Cyclic high fever with sweating and shivering; diagnosed by blood smear; treated with ACTs and quinine; controlled by nets, repellents, insecticides, draining stagnant water and the biocontrol fish Gambusia.
Amoebiasis (amoebic dysentery) — Entamoeba histolytica; faeco-oral route; diarrhoea, mucus and blood in stool, hepatomegaly; treated with metronidazole and tinidazole.
Ascariasis — Ascaris lumbricoides (nematode); through food and drink contaminated with eggs; larvae migrate through blood, heart, lungs, trachea, pharynx and back to the intestine; eosinophilia; treated with piperazine, mebendazole, levamisole, pyrantel.
Filariasis/Elephantiasis — Wuchereria bancrofti, Brugia malayi, Brugia timori; vector: female Culex; the worms block the lymphatic system, causing lymphedema, elephantiasis and hydrocele; incubation 8–16 months; treated with diethylcarbamazine citrate.
Typhoid — Salmonella typhi (Gram -ve; O antigen and H antigen); food- and water-borne; prolonged fever up to \(104\,^{\circ}\text{F}\), rose-coloured rash; diagnosed by the Widal test; treated with chloromycetin; prevented by the Ty21a (oral) and typhoid polysaccharide (injectable) vaccines.
Pneumonia — inflammation of the lungs/alveoli, caused by viruses (influenza, adenovirus, para influenza, RSV), bacteria (Streptococcus pneumoniae), fungi (Pneumocystis jirovecii, Pneumocystis carinii), or chemical/physical injury; spreads by contact and droplets; treated according to the causative pathogen.
Common cold (nasopharyngitis) — caused by a group of viruses (Rhinoviruses, Coronaviruses), which is why it recurs; Ring worm (dermatophytosis) — fungi of the genera Trichophyton and Microsporum that feed on keratin; Dengue — four related dengue viruses spread by the female Aedes mosquito, never directly from person to person.
Cancer — uncontrolled, purposeless division of cells forming a mass of undifferentiated cells (tumor/neoplasm). Benign tumors stay localized; malignant tumors grow fast, invade, and spread through blood or lymph to form secondary tumors (metastasis). Five main types: carcinoma (epithelial), sarcoma (connective tissue), lymphoma (lymphatic tissue), leukemia (blood/WBCs), adenocarcinoma (glandular tissue). Causes: chemicals, radiation, oncogenic viruses (v-onc genes), cellular oncogenes/proto-oncogenes (c-onc genes), and addiction. Treatment: chemotherapy, radiotherapy, surgery, immunotherapy (\(\alpha\)-interferon) and supportive therapy. Cancer specialists are oncologists.
AIDS — caused by HIV, a retrovirus (ss RNA) with reverse transcriptase, 100–140 nm, with matrix protein (p17), capsid protein (p24), a lipid coat with GP120 and GP 41. It destroys \(T_4\) (helper) lymphocytes, so immunity collapses and opportunistic infections appear. Spread by unsafe sexual contact, infected blood and needles, and from mother to child; not spread by casual contact. Four stages: initial infection → asymptomatic carrier state → AIDS related complex (ARC) → AIDS. Diagnosed by ELISA, confirmed by Western Blot; managed (not cured) by antiretroviral therapy (TDF, EFV, 3TC). First noticed in the USA in 1981; first Indian case in April 1986.
Adolescence (10–19 years) begins with the appearance of secondary sexual characters and ends with the cessation of body growth. Its three stages are early (10–14), middle (15–17; about 95 % of adult stature attained) and late (18–19). It brings a growth spurt, sexual development, and emotional and social changes. Mental illness is classified as psychoses or neuroses; treatment should preferentially be non-pharmacological, following WHO’s mhGAP guidelines.
Addiction is the compulsive use of a substance or repetition of a behaviour despite harmful consequences. It works through the brain’s reward and reinforcement pathways and the neurotransmitter dopamine — and, importantly, the neurological changes are reversible once use is discontinued.
Drugs abuse — the commonly abused drugs are opioids (heroin/smack = di-acetyl morphine, from Papaver somniferum; a depressant), cannabinoids (marijuana, hashish, charas, ganja, from Cannabis sativa; affect the cardiovascular system) and cocaine (from Erythroxylum coca; raises dopamine). Hallucinogens include lysergic acid and cannabis; Atropa belladonna and Datura spp. also have hallucinogenic properties. Repeated use raises receptor tolerance, leading to addiction and dependence, with a withdrawal syndrome (anxiety, trembling, nausea, sweating) if the drug is stopped abruptly. Effects include reckless behaviour, overdose and death, HIV and hepatitis B from intravenous use, cirrhosis of the liver, damage to the foetus in pregnancy, and the serious side-effects of anabolic steroids misused in sports. Prevention rests on avoiding undue pressure, education and counselling — with a special responsibility on parents and teachers.
Flowchart
FC 10.15 – The chapter in one sequence: Health (physical, mental, social well-being) → threatened by a pathogen → first met by innate immunity (barriers → complement and interferons → phagocytes and NK cells → fever → acute phase proteins) → if the pathogen persists, acquired immunity acts (antigen presented → helper T-cells → B-cells → plasma cells → antibodies; killer T-cells destroy infected cells) → memory cells retained → a second encounter is met faster and stronger → this same memory is used deliberately in vaccination → where prevention fails, disease results (communicable: malaria, amoebiasis, ascariasis, filariasis, typhoid, pneumonia, common cold, ring worm, dengue, AIDS; non-communicable: cancer) → health is also shaped by our own choices during adolescence → addiction and drug abuse → back to loss of health
10.8 Points to Ponder
WHO defines health as complete physical, mental and social well-being. Can a person living in a polluted, unsafe or hostile environment ever be called fully healthy, even if every medical test on them is normal? What does this suggest about who is responsible for a community’s health?
Innate immunity works within minutes but has no memory; acquired immunity takes days but never forgets. Why do you think evolution kept both, instead of perfecting one of them?
Suppressor T-cells exist to switch the immune response off. What would happen to a person in whom this brake failed? What does this tell you about the cost of a defence system that can attack anything?
Vaccination works because the immune system remembers. Yet a vaccine protects a community only when enough people take it. Where does an individual’s freedom to refuse end, and a community’s right to be protected begin?
Passive immunity acts at once but fades; active immunity is slow but lasts. If you were a doctor treating a patient bitten by a rabid animal, which would you give first, and why is that not a contradiction?
Group O is called the “universal donor” and group AB the “universal acceptor”. Are these labels completely safe in practice, given that the Rh system also exists? What could go wrong if a doctor relied on the ABO system alone?
An Rh-negative mother is given the very anti-Rh antibody we fear, in order to protect her future children. Explain to yourself why adding an antibody prevents the body from making that same antibody. Are there other situations in biology where interfering early prevents a larger response later?
Every disease in this chapter could be attacked at more than one point in its cycle — the pathogen, the vector, the route of entry, or the host’s immunity. For malaria, which point do you think is the most practical to attack in an Indian village, and why?
Ronald Ross found the malaria parasite in a mosquito more than a century ago, and we still have malaria. If we know the entire life cycle of the parasite, why has the disease not disappeared? What does this say about the difference between scientific knowledge and public health?
The genes that can turn a cell cancerous — the proto-oncogenes — are already present in every normal cell of your body. Why would a normal cell carry genes that are capable of destroying the organism? What might their ordinary function be?
Radiation causes cancer, and radiation is also used to treat cancer. Think about what makes the difference between the two situations. Can you find another example, in this chapter, of the same agent being both a danger and a cure?
HIV attacks the helper T-cell rather than any other cell of the body. Why does this single choice of target make the virus so much more dangerous than one that killed, say, a hundred times more cells of some other kind?
A person can be HIV positive, feel entirely well, and unknowingly transmit the virus for years. What does this long asymptomatic stage mean for the design of a public health programme? Is testing a medical act, a social act, or both?
People living with HIV often face stigma, although the virus does not spread by touch, sharing food, or sitting beside someone. Where does such fear come from, and what is the responsibility of a person who has studied this chapter?
Adolescence is described as a phase, not a fixed set of years. If two students of the same age are at very different points in this phase, how fair is it to expect exactly the same behaviour, maturity and performance from both?
Almost every listed cause of substance abuse in adolescence is about the environment around the young person — supervision, communication, rules, conflict, pressure — rather than about the drug itself. What does this imply about where the real work of prevention has to be done?
The neurological changes of addiction are reversible once the substance is discontinued. Why, then, is quitting still so difficult? And what does the reversibility tell us about how we should treat a person who is trying to quit?
An athlete who uses anabolic steroids gains strength but shuts down the body’s own hormone production. Is this a fair definition of “enhanced performance”? What is actually being borrowed, and who repays it?
10.9 Objective Questions
- Which of the following is NOT caused by unsterilized needles?
- Elephantiasis
- AIDS
- Malaria
- Hepatitis B
- Opium derivative is …………..
- Codeine
- Caffeine
- Heroin
- Psilocybin
- The stimulant present in tea is ………….
- tannin
- cocaine
- caffeine
- crack
- Which of the following is caused by smoking?
- Liver cirrhosis
- Pulmonary tuberculosis
- Emphysema
- Malaria
- An antibody is ……………
- a molecule that binds specifically to an antigen
- a WBC which invades bacteria
- a secretion of mammalian RBC
- a cellular component of blood
- The antiviral proteins released by a virus-infected cell are called …………
- histamines
- interferons
- pyrogens
- allergens
- Both B-cells and T-cells are derived from ………………..
- lymph nodes
- thymus glands
- liver
- stem cells in bone marrow
- Which of the following diseases can be contracted by droplet infection?
- Malaria
- Chicken pox
- Pneumonia
- Rabies
- The confirmatory test used for detecting HIV infection is ……………..
- ELISA
- Western blot
- Widal test
- Eastern blot
- Elephantiasis is caused by …………
- W. bancrofti
- P. vivax
- Bedbug
- Elephant
- Innate immunity is provided by ………..
- phagocytes
- antibody
- T-lymphocytes
- B-lymphocytes
- Match Column I with Column II.
| Column I | Column II |
|---|---|
| a. AIDS | i. Antibody production |
| b. Lysozyme | ii. Activation of B-cells |
| c. B-cells | iii. Immunoglobulin |
| d. T-helper cells | iv. Tears |
| e. Antibody | v. Immuno deficiency |
10.10 Check Your Concepts
Assertion (A): A person who has recovered from measles does not get measles again. Reason (R): Acquired immunity retains a memory of the first encounter with an antigen. Choose the correct option: both A and R are true and R explains A; both are true but R does not explain A; A is true and R is false; A is false and R is true. Justify your choice.
Assertion (A): Passive immunity acts immediately but is short lived. Reason (R): In passive immunity, the body’s own cells do not take part in producing the antibodies, and no memory cells are formed. State whether the assertion and the reason are correct, and whether the reason explains the assertion.
Why does the immune system need suppressor T-cells at all? What would you expect to happen in a person whose suppressor T-cells failed to function?
A vaccine contains a killed or weakened pathogen that cannot cause disease. Explain, step by step, how such a preparation still protects a person against the live pathogen.
Arrange the following in the correct sequence of events that occur when a bacterium enters the body through a cut: antibodies neutralise toxins; helper T-cells release lymphokines; the bacterium crosses the broken skin; plasma cells are formed; the antigen presenting cell displays the processed antigen; the B-lymphocyte is sensitised.
Draw a labelled diagram of an antibody molecule and label: heavy chain, light chain, disulfide bond, hinge, variable region, constant region and antigen binding site. Why is an antibody said to be bivalent?
Distinguish between an epitope and a paratope. On which region of the antibody is the paratope located, and why does that region have to be variable?
What would happen if a person of blood group A were given a transfusion of blood group B? Answer in terms of the antigens on the donor’s RBCs and the antibodies in the recipient’s serum.
Explain why group O is called the universal donor and group AB the universal acceptor. Why is this description still not completely safe in clinical practice?
An Rh -ve mother has already delivered one healthy Rh +ve child and is now pregnant with her second Rh +ve child. What risk does the second foetus face, and how can it be prevented? Explain why the first pregnancy was safe.
Why does an Rh -ve person have no anti-Rh antibodies before exposure to Rh +ve blood, while a person of blood group A has antibody ‘b’ in the serum without any previous transfusion?
Match the following.
| Column I | Column II |
|---|---|
| a. Plasmodium falciparum | i. Female Culex mosquito |
| b. Wuchereria bancrofti | ii. Female Aedes mosquito |
| c. Dengue virus | iii. Female Anopheles mosquito |
| d. Entamoeba histolytica | iv. Faeco-oral route |
| e. Salmonella typhi | v. Contaminated food and water |
Why does the fever of malaria recur at regular intervals of 48 or 72 hours in most species of Plasmodium, but at irregular intervals in P. falciparum?
In the life cycle of Plasmodium, meiosis takes place inside the mosquito. Using this fact, explain why the mosquito — and not the human being — is regarded as the definitive host.
What happens if stagnant water is allowed to collect around a settlement for several weeks? Name two diseases that could increase, and explain the biological link in each case.
Ascariasis is a disease of the intestine, yet some patients develop pneumonitis. Explain this apparent contradiction using the migration route of the larvae.
Explain, using the structure of the lymphatic system, why the limb of a patient with lymphatic filariasis swells to an enormous size.
A doctor treating a case of pneumonia says that antibiotics may or may not help. Explain why the same disease name can require completely different treatments.
Why do we catch a common cold again and again, but suffer from small pox or measles only once? Answer in terms of antigens and immune memory.
Ring worm is neither caused by a worm nor cured by an antibiotic. Explain both statements.
Assertion (A): All tumors are not cancerous. Reason (R): A benign tumor remains localized and does not undergo metastasis. Evaluate the assertion and the reason, and state whether a benign tumor can ever be fatal.
Proto-oncogenes are present in every normal cell of the body. Why, then, does everyone not develop cancer? What is the role of a carcinogen in this context?
Chemotherapy often causes hair loss and anaemia. Explain why these particular side effects occur, using the mechanism by which anticancer drugs act.
Radiation is listed both as a cause of cancer and as a treatment for cancer. Explain how the same agent can do both.
A patient with leukemia has a very high white blood cell count, yet is highly prone to infection. Explain this paradox.
HIV specifically destroys \(T_4\) (helper) lymphocytes. Explain why the loss of this one cell type damages both the antibody-mediated and the cell-mediated immune systems.
Most deaths in AIDS are due to “opportunistic infections”. What does the word “opportunistic” mean here, and why does it describe the situation accurately?
Why is ELISA used first and Western Blot used afterwards in the diagnosis of HIV infection? What is a “false positive”, and which of the two tests is meant to remove it?
An HIV test done a week after a possible exposure comes out negative. Explain why the person is still advised to be re-tested later. (Hint: think about what the test actually detects.)
Arrange the four clinical stages of HIV infection in the correct sequence, and state one characteristic feature of each.
A classmate refuses to share a bench with a student known to be HIV positive. Using the biology of HIV transmission, write what you would say to your classmate.
Adolescence is described as a phase and not a fixed number of years. Explain what this means, and why two 15-year-olds may be at very different points in it.
Distinguish between the early, middle and late stages of adolescence with respect to (a) physical growth, (b) type of thinking, and (c) the role of the peer group.
Explain the difference between a hallucination and an illusion, and give one example of each.
Distinguish between tolerance, dependence and addiction. Which of the three explains why an addicted person keeps increasing the dose?
What happens if a person who is dependent on a drug abruptly stops taking it? Name the condition and list its characteristic signs.
Explain how an addictive drug hijacks the brain’s reward pathway. Why is it significant that the resulting neurological changes are reversible?
A male athlete misusing anabolic steroids finds that his testes have shrunk and his sperm count has fallen. Explain this using the idea of hormonal feedback.
Almost every listed cause of substance abuse during adolescence concerns the environment around the adolescent rather than the drug itself. What does this tell you about where preventive effort should be directed? Support your answer with two examples from the list.
Why are those who inject drugs intravenously at a high risk of HIV and hepatitis B? Link your answer to the body fluids in which HIV is present in the greatest concentration.
What is the source of cocaine? (30–40 words)
Name one disease caused by smoking. (30–40 words)
Which cells stimulate B-cells to form antibodies? (30–40 words)
What does the abbreviation AIDS stand for? (30–40 words)
Name the causative agent of typhoid fever. (30–40 words)
What is the Rh factor? (30–40 words)
What is a schizont? (30–40 words)
Name the addicting component found in tobacco. (30–40 words)
Name the pathogen causing malaria. (30–40 words)
Name the vector of filariasis. (30–40 words)
Give the name of the causative agent of ringworm. (30–40 words)
Define health. (30–40 words)
What are acquired diseases? (80–100 words)
Differentiate between antigen and antibody. (80–100 words)
Name the infective stage of Plasmodium. Give any two symptoms of malaria. (80–100 words)
Explain the mode of infection and the cause of elephantiasis. (80–100 words)
Why is smoking a bad habit? (80–100 words)
What do the abbreviations AIIMS and CMIS denote? (80–100 words)
What is a carcinogen? Name one chemical carcinogen with its target tissue. (80–100 words)
Distinguish between active immunity and passive immunity. (80–100 words)
Differentiate between B-cells and T-cells. (80–100 words)
What are the symptoms of malaria? How does malaria spread? (80–100 words)
Write a short note on AIDS. (80–100 words)
Give the symptoms of cancer. (80–100 words)
Write a note on antigens on blood cells. (80–100 words)
Write a note on the antigen–antibody complex. (80–100 words)
What are the various public health measures that you would suggest as a safeguard against infectious diseases? (80–100 words)
How does the transmission of each of the following diseases take place? (80–100 words)
- Amoebiasis
- Malaria
- Ascariasis
- Pneumonia
What measures would you take to prevent water-borne diseases? (80–100 words)
Write a short note on typhoid. (80–100 words)
Describe the structure of an antibody. (150–200 words)
Write a note on vaccination. (150–200 words)
What is cancer? Differentiate between a benign tumor and a malignant tumor. Name the five main types of cancer. (150–200 words)
Describe the different types of immunity. (150–200 words)
Describe the ill-effects of alcoholism on health. (150–200 words)
In your view, what motivates youngsters to take to alcohol or drugs, and how can this be avoided? (150–200 words)
Do you think that friends can influence one to take alcohol or drugs? If yes, how may one protect himself or herself from such an influence? (150–200 words)