CSIR NET Ch 4A

8/2/2019 CSIR NET Ch 4A

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*MUDRA* Life Sciences For NET & SET Exams. Of UGC-CSIR

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Section B & C Vol-06

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Section B and C

Volume-06

Contents

4. CELL COMMUNICATION AND CELL SIGNALING

A. HOST PARASITE INTERACTION 1

B. CELL SIGNALING 19

C. CELLULAR COMMUNICATION 69

D. CANCER 101


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4. CELL COMMUNICATION AND CELL SIGNALING

A. HOST PARASITE INTERACTION

Mode of Transmission and alteration of host cell behavior by pathogens:

Every infectious disease is transmitted to humans from its reservoir by a characteristic

mode of transmission. The most common modes are

(1) Ingestion of food or water contaminated by faeces (the oral-faecal route),

(2) Contamination of the respiratory tract by droplets or other material containing

respiratory secretions (the respiratory route), and

(3) Direct contact with another person, animal, or contaminated object. Another

important mode of transmission is inoculation through the skin when a wound is produced by an

inanimate object or, by the bite of an arthropod or mammal.

Bacterial pathogens

One of the great, achievements of medical science, occurring in this century, was the

discovery of therapeutically effective anti-bacterial drugs. Now, nearly all bacterial diseases can

be cured if an accurate diagnosis is made early in the course of the infection. In the following

discussions of the principal human bacterial diseases, emphasis is placed on features important in

their recognition and control.

TABLE:1. PATHOGENIC GRAM POSITIVE BACTERIA

Group of Pathogenic bacteria Disease Caused

Nocardioform bacteria

Corynobacterium diphtheriaeMycobacterium bovis

M. leprae

M. tuberculosisNocardia anteroidea

Endospore forming bacteria

Bacillus anthracisClostridium botulinumC. diffelle

C. perfringene

C. tetani

StaphilococciStaphilococcus aureus

DiphtheriaTuberculosis

Leprosy

TuberculosisInfection in immunodeficient individuals

AnthraxBotulism

Pseudomembranus colitis

Gangrene

Tetanus

Impedigo, boile, wound infections,

pneumonia, toxic shock syndrome


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Staphylococcal Diseases

Nearly all human staphylococcal diseases are caused by Staphylococcus aureus, a

facultatively anaerobic coccus that produces clumps of cells as it grows. It occurs on the skin and

nasal passages of healthy humans and domestic animals. Approximately, 50 percent of these

strains produce a heat-stable enterotoxin that causes food poisoning when ingested. S. aureus can

also cause a wide variety of infections that are described as pyogenic (pus-forming). Examples

include impetigo, boils, wound abscesses, and pneumonia. Impetigo is a superficial skin

infection that is common in children and occasionally occurs in adults; boils (furuncles) are

abscesses that form in hair follicles.

Pathogenic staphylococci produce a number of extra-cellular proteins that are important

in pathogenesis, including coagulase, leukocidin, and haemolysin. Coagulase initiates formation

of blood clots that can protect bacteria from phagocytosis. Leukocidins are cytotoxins that kill

leukocytes; haemolysins are cytotoxins that lyses red blood cells in vitro and are also toxic to

leukocytes.

Streptococcal Diseases

Two species of streptococci, S. pyogencs and S. pneumoniae, cause most human

streptococcal disease. The human population is the reservoir of these two species of facultatively

anaerobic cocci that grow in chains. S. pneumoniae, commonly calledpneumococcus, is present

in the upper respiratory tract of most healthy individuals, but S. pyogenes is rarely present in

healthy people.

The most important pneumococcal diseases are pneumonia, otitis media (infection of the

middle car), and meningitis (infection of the membranes surrounding the brain). Immunity

depends on production of an antibody that binds specifically to pneumococcal polysaccharide.

The most common diseases caused by S. pyogenes are impetigo (which is similar in

appearance to the impetigo caused by Staphylococcus aureus), and streptococcal pharyngitis

(streptococcal sore-throat). Many strains ofS. pyogenesproduce, both extracellular enzymes that

break down host macromolecules and streptoldnases, enzymes that activate a host factor that

dissolves blood clots. It has been suggested, but not proven, that these enzymes facilitate the

spread of streptococci. Most strains also produce the cytotoxins, streptolysin and streptolysin S

that kill host leukocytes and red blood cells, thereby contributing to the pus formation,


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characteristic of streptococcal disease. Strains that secrete these streptolysins can be readily

identified; because, they produce clear zones of lysis, termed -haemolysis, when grown on

blood agar. Some other streptococci produce, by an unknown mechanism, small zones of partial

haemolysis, termed -haemolysis. Some strains secrete also a toxin termed erythrogenic toxin

that produces the characteristic rash of scarlet fever. There are three distinct types of

erythrogenic toxin, and the gene encoding each is carried on the chromosome of a temperate

bacteriophage. Immunity to S. pyogenes depends on antibodies that bind to a protein, termed M

protein, that is located on the cell surface and that inhibits phagocytosis. There are more than 50

antigenically distinct types of M protein, and immunity to one type docs not protect the host

from infection by another.

Streptococcal pharyngitis is, occasionally, followed by post-streptococcal glomerulo-

nephritis, a disease characterized by temporary kidney failure, apparently caused by immune

complexes (produced from fragments of streptococcal walls cross-linked by antibodies) that

become lodged in the glomeruli of kidneys. Streptococcal pharyngitis can also be followed by

rheumatic fever, a disease, characterized in part, by an enlargement of the heart and temporary

arthritis. In turn, rheumatic fever m some cases is followed by a more serious disease, rheumatic

heart disease. Although it is clear that streptococcal infection plays a role in causing these two

diseases, the mechanisms involved are not understood.

Diseases caused by Endospore-Forming Bacteria

The diseases caused by various endospore-forming bacteria. One of these, anthrax, which

was studied by R. Koch, and by L. Pasteur, is primarily a disease of sheep. Rarely, it affects

humans when spores of the causative agent, Bacillus anthracis, enter a wound or are inhaled. In

the latter case, they cause a severe pneumonia termed woolsorters disease.

Clostridial gangrene develops in necrotic (dead) tissue that has lost its blood supply. As a

consequence, spores of certain obligate anaerobes, often Clostridium perfringens, can germinate

and vegetative cells can proliferate there. As they do, they secrete hydrolytic enzymes and

cytotoxins that kill and digest surrounding host cells, expanding the necrotic area in which the

clostridial cells grow. Antibiotics are of little use in the treatment of gangrene; because, without

a blood supply in the affected tissue, there is no effective way to get them into the site of

infection.

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CSIR NET Ch 4A