Infections And Microorganisms That Causes Throat Disorder Biology Essay


Sore throat is a common symptom of many physical disorders and is caused by virus, bacteria and yeast. Sore throat is the inflammation in mucous membrane linings which may be painful. It is a transferrable disease and it is common in winter season because the upper respiratory infections are more frequent due to cold [3.1]. This infection may cause a group of people or members of one family at a single time. Sore throat may be of two types either acute sore throat or chronic sore throat. When sore throat is caused by bacteria, it is called as strep throat. The difference between the viral and bacterial sore throat is that the viral infection does not respond to antibiotics where as the bacterial infections can be cured by antibiotics.

Review of literature

Sore throat is the most common symptom of various physical disorders which can also caused by the bacteria and virus. The main causes of the sore throat are common cold, flu, mononucleosis, continuous breathing by mouth, chronic tonsillitis, diphtheria, sinusitis and smoking. Medically sore throat is known as pharyngitis. Sore throat may be of two types - acute sore throat and chronic sore throat. When the sore throat lasts for less than seven days or gets cured within eight days then it is termed as acute sore throat and when the sore throat remains up to three weeks or even more, it is called as chronic sore throat [3.1].

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Tonsils are the fleshy clusters of soft tissues present behind and above either side of the tongue. The inflammation of tonsil is known as tonsillitis. During tonsillitis, the adenoids and lingual tonsils are inflamed; hence tonsillitis is otherwise known as pharyngitis [2]. Tonsil is a part of immune system which helps and protects body to fight against the infection. It has many lymph nodes that produce antibodies during the invasion of bacteria and virus into the body. Tonsillitis is common in children because of immature immune system. The bacteria and viruses are main causing agent of tonsillitis. It is a transferrable disease. When tonsillitis caused by bacteria can be cured by antibiotics however, when it is caused by virus, antibiotics do not make the grade.


Due to the viral and bacterial infection and poor immune system, tonsils get inflamed; a condition known as tonsillitis. During tonsillitis the tonsil turn red, enlarged and have a whitish or yellowish coating on the surface of it. The symptoms of the tonsillitis are:-


Severe sore throat.

Difficulties during swallowing food.

Change in voice.


The main causative agents of tonsillitis are bacteria Streptococcus pyogenes and virus Epstein Barr Virus.

Figure 1: inflammation in tonsils

Complexities in tonsillitis

Acute tonsillitis: It is the sudden and severe inflammation in the throat on the area of lymph tissues present behind and above the tongue. This can be cured by the oral steroid and antibiotics. This mainly caused by the streptococcus bacteria. This happens during kissing or comes in contact with mucus of person carry streptococcus bacteria [6].

Chronic tonsillitis: It is a continuous recurring infection in tonsil. As this infection is repetitive so the pockets or crypts like structures are formed in the tonsil where bacteria can store due to which small, foul smelling stones made up of sulfur are found which is known as tonsillitis. The symptoms of this infection are disturbed sleeping, foul breathe, changes in voice [5]. Tonsillectomy: It is the surgical removal of tonsil to avoid the repetitive occurrence of tonsillitis [2].

Gluear: Adenoid is a part of lymph nodes in tonsil, consequently during tonsillitis adenoid is also swollen which block the Eustachian tube (a thin tube connects back of the throat to middle air). Due to the block of Eustachian tube, various sticky fluids is formed inside the tube which interferes with hearing [2].

Quinsy: It is otherwise known as peristalsis abscess. A collection of pus is known as abscess. Pus formation occurs by the bacterial infection in the crypts on the surfaces of tonsil. The pus formation is due to the infectious WBC and the cell debris that looks like a whitish or yellowish layer on the surface of tonsil. This infection creates severe pain in tonsils [3].

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Figure 2: Quinsy


The infections of S. pyogenes usually begin in the mouth and upper respiratory parts. A group of S. pyogenes enters into the mouth during inhalation when someone come contact with infected person. Many S. pyogenes are destroyed by the stomach juices during swallowed and remain microbes are digested by lysozyme enzyme in saliva that degrades the outer peptidoglycan layer of S. pyogenes. After digesting of microbes by stomach juices and lysozyme still some microbes are remains by attaching to the surface of throat using lipoteichoic acid present on their cell wall. Many of them are repelled by secretory IgA antibody in saliva that cross-reacts with antigens on their surface. However, some of them are successful in gaining a loose attachment in the throat and they bind more tightly to the epithelial cell surface of throat by the help of fibronectin present on the epithelial cell surface and M protein on the microbe (M protein is present on the cell wall surface of S. pyogene which is virulence in nature. The function of M protein is it inhibits opsonization by the alternative complement pathway by binding to host complement regulators). After binding, the microbes begin to multiply and increase in population. Multiplication of S. pyogene occurs by the low pH created by normal flora and the presence of β-lysins. The colonies start to expand and invade layers below the epithelial cells [4].

S. pyogenes starts secreting a damaging enzymes Hyaluronidase into the surrounding tissues of the host. Hyaluronidase enzyme degrades the hyaluronic acid. The hyaluronic acid cements cells together in many mammalian systems, allowing further invasion. The secretion of DNase, RNAse and proteases are also aid to the microbe. This internal damaging causes the secretion of chemicals like chemokines and bradykinin from ruptured or damaged cells, thus the process of inflammation occur. Bradykinin which secrete from damaged cells binds to receptors in blood vessel cells in nearby capillaries and forms gaps in the walls of blood vessel. Chemokines and Microbial products from damaged cells leak into the surrounding area and into the bloodstream, attracting the attention of phagocytes mainly neutrophils and macrophages, then these phagocytes start migrate into the area of infection by S. pyogene [4].

As the bacterium secretes several proteins like leukocidins which are toxic to phagocytes so at this point the phagocytic attack is inefficient. S. pyogenes is also surrounded by a capsule made of hyaluronic acid, the same compound cementing human cells and this makes the microbes difficult to recognize. This capsule is also attacked by hyaluronidase made by the pathogen, but they able to make enough of it which is still protective. The capsule makes phagocytosis difficult which leads to the slow rate of phagocytosis that is the reason why the number of bacteria continues to increase. The body attacks to wall off the infection by encasing in a fibrin clot, but streptokinase produced by the microbe dissolves the clots which further leads the infection forward [4].

As the number of S. pyogene increases, greater numbers of macrophages, neutrophils and dendritic cells penetrate the area of infection. Active phagocytosis causes the release of more mediators of inflammation and the inflammatory response intensifies, then there is soreness at the back of throat occur. Neutrophils are filled with bacteria, they die and make up the pus on the surface of the throat and causes the characteristic yellow or whitish spots on the surface of throat. The above causes such as inflammation of tonsil, soreness in throat, formation of pus on the surface of throat all together cause tonsillitis [4].


Tonsillitis [online] (updated 11th February 2009) Available at: [accessed 11th October 2010].

Shah, U.K, 2009. Tonsillitis and Peritonsillar Abscess, Emedicine from webMD

Quinsy [online] Available at: [accessed 11th October 2010].

Microbial pathogens [online] Available at: [accessed 20th October 2010].

Tonsillitis [online] Available at: [accessed 20th October 2010].

Acute tonsillitis [online] Available at: [accessed 20th October 2010].



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Diphtheria is an infectious upper respiratory disease mainly caused by the toxin of Corynebacterium diphtheriae bacteria. C. diphtheria is living in mouth, nose and skins of the infected person. This disease is characterized by sore throat, mild fever, and an adherent membrane formed on tonsil. Usually it affects the throat and nose and in more serious cases, it can affect the heart and nerves. It is a contagious disease spread by direct physical contact or respiratory droplets from the throat through coughing and sneezing of an infected person. The toxin production is due to specific viruses that carrying the genetic information for toxin (tow gene) which infects the bacillus [2].


Corynebacterium diphtheria: Corynebacteria are Gram-positive, rod-shaped, aerobic, non-motile, bacteria classified as Actinobacteria. Corynebacteria are related phylogenetically to actinomycetes and mycobacteria. They have the characteristic of forming irregular or V-shaped arrangements in normal growth. The genus Corynebacterium consists of a group of bacteria including plant and animal microbes or pathogens. Some corynebacteria are part of the normal life of humans, finding a suitable place in virtually every anatomic site, especially the skin and nares. A very popular and widely known bacterium is Corynebacterium diphtheriae which causes the disease Diphtheria [4]. The main symptoms of the diphtheria are:-

Mild fever

Sore throat

A membrane formed on the surface of tonsil and throat which cause difficulties during swallowing

The bacteria can infect any of the mucous membranes and have 2-5 days incubation time. The diphtheria infection occurs in different parts of the body and varies in severity of pain. Mainly it causes the infections in tonsils, pharynx, and sometimes it may invade the nasal tissues, larynx and skin. Tonsillar, Pharyngeal and laryngeal diphtheria are more severe as compare to other type of diphtheria because more amount of toxins are absorbed by blood serum. The pseudomembrane is a fibrin network infected by multiplying C. diphtheriae cells which grows over a necrotic lesion on the epithelial cells on the surface of the throat. The consequences of this membrane may be severe if the membrane grows up to much extent which blocks the air ways in throat [3].

The result of the disease depends on quantity of toxin is absorbed into the bloodstream. The toxin has degenerative effects on the kidneys muscles, spleen, heart, nerves, and liver. In the most severe cases, an infected person will develop myocarditis (inflammation of heart muscle) or neuritis (damage in nerves), which leads to heart failure and local paralysis most commonly of the soft palate [2].


Usually all the strains of C. diphtheriae don't have toxic because the gene for diphtheria toxin (DT) is not found in the genome of bacteria. Mainly in the genome of a corynephage (virus) DT gene is located. The toxinogenicity of Corynebacterium diphtheriae depends upon the phage which contains a functional gene for the toxin protein. Usually some few phages have the DT gene tox, so the C. diphtheria may undergo for lysogenic conversion or be infected by a phage, without producing DT [1].

C. Diphtheria produces the diphtheria toxin as a single protein. Technically this DT is a proenzyme, as it is cleaved by bacterial proteases into 2 fragments i.e. A of molecular weight 21,150 and B of molecular weight 39,000. Fragment A is the sole source of toxicity of DT and is catalytically active. Fragment B have no enzymatic activity and is less stable than the active fragment A. After entering the toxin into the host cell each fragment plays different roles. Diphtheria toxin enters into the host cell by binding to the extracellular EGF domain of the heparin-binding epidermal growth factor precursor (HB-EFG precursor). Then this binding produces a hydrophobic domain of the fragment B to create a channel across the membrane through which fragment A can pass into the cytoplasm. Fragment B contains the receptor binding and transmembrane domains of the toxin, which remains on the plasma membrane [1].

DT is an ADP-ribosyl (ADPR) transferase. The toxicity of DT comes from stopping protein synthesis in the host cell by disabling EF-2 or cellular elongation factor. EF-2 is an important part of the process of translation. Fragment A is free in the cytoplasm and catalyzes the reaction as below:

EF-2 + NAD+ --> ADPR-EF-2 + nicotiamide + H+

The above reaction produces a covalent bond between EF-2 and ADPR that blocks the functional site which interacts with RNA in translation, and consequentially stopping all protein synthesis at a particular ribosome.

The structural gene of DT is in the phage chromosome and the gene expression is controlled by DtxR gene on the corynebacterium diphtheriae chromosome. Usually expression of tox gene is inhibited by negative feedback by the DTxR gene product. The levels of iron in the surrounding tissue environment have a significant effect on the DTxR gene expression and consequentially on DT production. The low levels of iron inhibit the DTxR gene expression which helps in stopping the negative feedback loop inhibiting tox gene expression. If the corynebacterium diphtheriae bacteria are grown under certain severe iron-deficient conditions, DT protein can make up about 5% of all protein being synthesized. So iron refers as a co-repressor with DTxR to prevent the expression of DT production [3].

Figure 3: Mechanism of action of C. diphtheria toxin in diphtheria disease.


Background Information and Life Cycle [online] Available at: [accessed 14th October 2010].

Diphtheria (Corynebacterium diphtheriae) [online] Available at: [accessed 14th October 2010].

Analysis of the molecules and receptors involved in bacterial infection [online] Available at: [accessed 14th October 2010].

Diphtheria [online] [accessed 14th October 2010].



the irritation and inflammation in pharynx or in throat is known as pharyngitis. When pharyngitis occurs for short period of time then it is called as acute pharyngitis. This is caused by both virus and bacteria, but in most cases it causes by virus. The bacteria responsible for this disease are group A, C, G and F streptococci [2]. When pharyngitis is caused by the above mentioned group of streptococci bacteria then it called as streptococcal pharyngitis. The symptoms of pharyngitis are same as strep throat such as tonsillitis, sneezing, cough, fever. This diseases is more common in those people who are subjected to or suffer from allergies, chronic sinusitis, smoking, closely contact with pharyngitis patient. Acton of mechanism of group A and C Beta-Hemolytic Streptococci in pharyngitis are same as s. pyogene in tonsillitis as tonsillitis is otherwise known as tonsillitis


Group C beta-hemolytic streptococci causing pharyngitis and scarlet fever [online] Available at: [accessed 15th October 2010].

Causes of pharyngitis [online] Available at: [accessed 15th October 2010].

Causes of Sore Throat or Pharyngitis [online] Available at: [accessed 15th October 2010].

Microbial pathogens [online] Available at: [accessed 15th October 2010].



Epstein Barr Virus (EBV) is a very common virus which causes many infectious diseases. This virus is from Herpes family so it is otherwise known as Human Herpes virus (HHP). The EBV has a double-stranded linear DNA core surrounded by nucleocapsid and an envelope that contains glycoproteins as the genetic material which multiplies in the human lymphocytes and other cells. It mainly causes the disease infectious mononucleosis which has the side effects like sore throat, pharyngitis and lymphadenopathy. It is a contagious disease. These EBV are mainly present in human saliva. So it is highly transferrable during oral kissing and sharing food. It is also rarely involved in development of different uncommon types of tumors such as tumors in throat and nose [1].

Review of literature

The EPV are usually found on the line of lymphocytes of the human body, but they do not harm anything and body also not eliminating those germs, this is known as latent infection [1]. It causes the disease infectious mononucleosis whose symptoms are:-

Sore throat

Swollen in lymph glands


Pus like substances present on surface of throat

Sometimes swollen occur in lever or spleen

If a person was previously suffering from EBV infection or infectious mononucleosis, then he/she has a low risk of being attacked by EBV infections the next time. The transfer of this infection needs intimate contact with saliva. It does not transfer through air or blood. The incubation period of this virus i.e. the time between the infection and appearance of symptoms takes 4-6 weeks hence the person with infectious mononucleosis are able to spread the infection up to 30-40 days. This EBV creates a dormant (inactive but capable of becoming active) infection in some cells of immune system of body. The infection becomes chronic when it remains in the body for a period more than six months [2]. During the infection of EBV they specially infect the white blood cells of human body. EBV remains in the body, mainly in white blood cells, after the first infection. Sometimes the viral genes change the growth cycle of infected cells which cause them to become cancerous which leads to tumors in throat [3].

There are no special precautions available for mononucleosis because the EBV remains in the saliva of healthy people, which can be easily transferrable to other people. The diagnosis of mononucleosis is done on the basis of symptoms.


The EBV has two distinct phases of life. Firstly, it goes into a resting phase after infecting a cell. During the suitable circumstances the virus become active and it promotes its synthesis inside the cell especially in patients with weakened immune systems [5].

A viral protein named BZLF1 activates the EBV genes, which is essential for the growth and multiplication of virus particles. About 70 different genes are switched off at the time of latent phase because certain DNA segments are chemically modified; in the sense the building blocks of DNA carry the methyl group which works like stop signal for cell apparatus so these genes cannot convert into proteins. But the BZLF1 protein can detect these methylation patterns in DNA and bind with that by its DNA binding domain and the 2nd domain of BZLF1 is responsible for reactivation of gene [5].

During the lytic cycle of EBV, it produces a large no. of new viral particles within the cell. For achieving this, viruses use a huge portion of the cell apparatus, in particular specific proteins and factors. Thus the viruses activate the immune system of the host, which fights against the pathogens and destroy the cells which are supporting viral synthesis [5].

At this time the EBV uses another strategy i.e. Instead of using all its energy in immediate synthesis of progeny inside the infected cell; it goes into a resting phase following the infection and thus prevents the reaction of the immune system [5].

The EBV infects the cells of the immune systems i.e. B cells by transferring its DNA into B cell nucleus, whereas many viruses immediately start their lytic proliferation cycle by using the cell apparatus for replication of DNA and produces essential structural proteins from the genes. EBV drives transformation of about a few genes from the cell into proteins which are called as latent genes. These latent genes are important for the quiescent phase. They see to it that the DNA of the Epstein-Barr virus remains stable in the cell nucleus while the cell itself proliferates. Sometimes it causes tumors [5].

Figure 4: Epstein Barr Virus

Simple mechanism:-

Mainly the EBV is present in the human saliva. So initially the EBV enters trough saliva into the crypts of lymphoepithelial structures of tonsil [4].

Then it crosses the epithelial barrier which is of thickening of cells just above the bed of lymphocytes below [4].

EBV infects the unaffected B cells and drives them to become blast through expression of the growth program under the regulation of EBV nuclear antigen 2 (EBNA2) [4].

EBV-infected blasts switch from the growth program to the default program by disabling EBNA2. In the absence of EBNA2 Expression of latent membrane protein (LMP1) and LMP2A (B cell receptor homologue) provides the requisite survival signals [4].

EBV latently infected resting memory cells left the follicles and enter the peripheral circulation through the efferent lymphatics. The EBV-infected cells express very little or no genetic information; therefore it is non-pathogenic and not recognized by the immune response which may maintain as normal memory cells [4].

From the peripheral circulation Memory cells re-enter the tonsil through high endothelial venules [4].

Survival of antigen-specific memory cells requires an unaffected B cell receptor. EBV infected memory cells express the default program which might provide the necessary signals for long term survival of the cells as memory cells. Then they turn off the default program, and leave by the efferent lymphatics [4].

Occasionally, a small quantity of latently infected memory cells initiates replication of the virus to be shed into saliva. Failure to activate the default program before LMP1 and LMP2A protein are lost might be the trigger [4].

Figure 5: pathways of Epstein-Barr virus exploiting the immune system


Epstein Barr Virus infection causes [online] Available at: [accessed 12th October 2010].

Epstein - Barr virus and Infectious Mononucleosis [online] Available at: [accessed 12th October 2010].

Epstein - Barr virus (EBV) Infection [online] (updated February 2007) Available at: [accessed 12th October 2010].

Hypothetical model of how EBV persistence [online] Available at: [accessed 12th October 2010].

Key mechanism for the proliferation of Epstein-Barr virus discovered [online] Available at: [accessed 12th October 2010].

BZLF1-ir is the transcriptional activator that mediates the switch between the latent and lytic forms of EBV infection.

LMP1-it is an oncogene of EBV and involved in EBV associated tumors.

Yeast throat infection


Yeasts are the eukaryotic unicellular microorganisms classified in kingdom fungi. These are commonly remains in the human gastrointestinal tract and at the moist and warm areas of the body like oral cavity, mucus membrane. Yeast infections are commonly called as thrush or Candidiasis. Mainly the yeast named Candida Albicans causes the infection in throat as well as other parts of the body [1]. These microscopic germs do not harm the body when their populations are kept controlled by healthy immune system and the beneficial bacteria (Bifidobacteria bifidum and Lactobacillus acidophilus) found in the body. Candida is the part of ecological balance in the human body. When the immune system is not strong the no. of beneficial bacteria get reduces due to some underlying factors, during this time the yeasts are multiplied rapidly in the body which leads to yeast infection. This Candida infection may spread several parts of the body [1].


Throat infections can be caused by virus, bacteria and fungi or yeasts. When the throat infection causes by yeast or fungi then it is called as thrush or candidiasis. This candidal infection commonly affects when there is deficiency in immune system in the body. It is a communicable disease. Highly it is transferable during the oral sex. So the person affected in candidiasis should stay far from sex otherwise his/her partner will also suffer in same disease. [2, 5].

The symptoms of this disease are ranging from mild to severe such as:-

Reddening in throat.

Swelling of throat that persists for a long time.

Slightly raised whitish or yellowish lesions in the throat which are painful and may bleed.

Experiencing soreness in throat.

Difficulties during swallowing food.

Patient suffering from this disease may also suffer in stomach upset.

People with weakened immune system, diabetes and other metabolic disorders, as well as those taking more antibiotics, steroid drugs and undergoing cancer treatments like, chemotherapy have a greater risk of developing yeast throat infection. This is why the HIV/AIDS patients are more likely to have the severe yeast throat infection. Immune deficiencies in body occur due to several physical disorders, rapid taking of steroid drugs and antibiotics. Taking of more antibiotics kill the beneficial bacteria which leads to rapid growth of yeast, so yeast infections occur [4].

The cure for a throat yeast infection can be done by the antifungal medicines. Also, adding good bacteria is crucial in the treatment of throat yeast infection. This is done to help both the immunological response and get the best out of beneficial bacteria.


Mainly the yeast infection cause in throat due to the deficiency in immune system and rapid taking of antibiotics, steroid drugs etc. Deficiency of immune system occurs due to the many physical disorders in health such as stress, lack of sleep, taking steroid drugs etc. As long as the immune system is healthy and strongly functioning Candida albicans growth is regulated and kept under control by some beneficial bacteria. When there is deficiency in immune system the environment of the beneficial bacteria (Bifidobacteria bifidum and Lactobacillus acidophilus) becomes imbalance so there occurs in reducing the no. of beneficial bacteria which leads to rapid growth or multiplication of the Candida albicans. Candida albicans produce the endotoxins during their reproduction and death which is virulent in nature. Due to the virulence nature of endotoxins cause local irritations and damaging of tissue surfaces which allow the penetration of monilia into the dip of the tissue and blood this causes the infections in throat or candidiasis [1, 3].

Deficiency in immune system

C. albicans present in body under control growth.

Rapid growth of C. albicans

Rapid taking of steroids and antibiotics

Production of endotoxins by reproduction and death of c. albicans

C. albicans penetrate into the dip of tissue and blood.

Endotoxins damage the surfaces of throat tissues.


Pathway of C. albicans causes throat infection or candidiasis


Throat yeast infection [online] (updated 15th march 2010) Available at: [accessed 7th October 2010].

SarahLeaRhodes, 2010. Yeast Infection in the Throat - Dangerous Illness You Cannot Ignore, Health and Fitness.

Seelig, M.S., 1966, Mechanisms by Which Antibiotics Increase the Incidence and Severity of Candidiasis and Alter the Immunological Defenses, American Society for Microbiology, 30(2), pp. 442-454.

Yeast Infection of Throat - Causes and Symptoms [online] Available at: [accessed 7th October 2010].

Throat Yeast Infection Treatments, Causes and Symptomshttp [online] Available at:

Adenovirus causing throat infection


Adenoviruses are the medium sized (60-90 nm in diameter) naked virus composed of nucleocapsid and double stranded nuclear DNA. The human adenovirus belongs to the Mastadenovirus genus. These viruses mainly cause the upper respiratory tract infections such as cold, pharyngitis, inflammation in throat etc., also it causes the infections like acute diarrhea, conjunctivitis, pneumonia. Patients with poor immune system are especially susceptible to severe adenovirus infection. There are about 51 human adenovirus which are divided into subgroups (A-F) based on their capacity agglutinate erythrocytes of human. The infections caused by adenovirus are more contagious [1.3].

Review of literature

Physiology of adenovirus:

All the adenovirus particles are of similar size. They have icosahedral symmetry which can be easily visible with the help electron microscope by negative staining. They are composed of 240 hexons, 252 capsomers, and 12 pentons at vertices of icosahedron. Hexons are consisting of a trimer of polypeptide II and a central pore with minor proteins VI, VIII and IX. Pentons are more complex molecules consist of a pentamer of peptide III and 5 molecules of IIIa associated with the penton base. It has a toxicity activity. A trimeric fibre protein is extends from each of the 12 vertices i.e. attached to the penton base proteins which is responsible for recognition and binding to the cellular receptor. A globular domain present at the end of the adenovirus fiber is responsible for recognition of the cellular receptor. The Linear, non-segmented, double stranded DNA, 30-38kbp which has the theoretical capacity to encode 30-40 genes. Serotypic origin of the E1A gene determines the oncogenic phenotype of adenovirus-transformed cells. Viruses belonging to subgroup A i.e. adenovirus 12 and Ad12 are induce tumors with high frequency and short latency, where as the viruses from subgroup B (Ad3 and Ad7) are weakly oncogenic. Subgroup C (Ad2 and Ad5), D, E and F of the adenoviruses are non-oncogenic [1].

The signs and symptoms of the adenovirus infection are:




Swollen lymph nodes



Figure 6: Adenovirus


All viruses are obligate intracellular parasites and cannot multiply outside the host cell. Adenoviruses are highly stable outside the host cell and can maintain infectivity at room temperature for 2 weeks, after freezing at 39°F (4°C), and at a pH ranging from 5 to 9. They can be destroyed by heating to 129°F (54°C) for 30 minutes, standard disinfectants and detergents used for cleaning noncritical environmental surfaces, or hand hygiene agents. Adenoviruses infect the host cell by attachment, using a capsid protein, and subsequently are internalized by receptor-mediated endocytosis. The endosome is disrupted by the virion, allowing the DNA to enter the nucleus of the host cell, where replication occurs. Replication begins as early as 5 hours after infection and is associated with inhibition of cellular and protein synthesis. In permissive cells, about 104 virions per cell may be produced over the next 48 hours. Ultimately, host cell protein synthesis comes to a halt and cell death occurs which leads to infection [2, 3].

Normal Steps during the adenovirus infection in throat

Attachment on the cell surface of host.

Penetration into the cell.

Uncoating the outer layer of virus.

Passing the genetic material of virus into nucleus of the cell through nuclear pore.

Replication of viral DNA.

Figure 7: Action mechanism of adenovirus infection.


Adenoviruses [online] Available at: [accessed 19th October 2010].

Respiratory adenovirus [online] Available at: [accessed 19th October 2010].

Langley, J.M, 2005, Adenoviruses, infectious diseases 26(7), pp. 244-248.



Croup is an upper respiratory infection causes the inflammation in throat or upper airways and sometimes it creates problems in breathing. It is a viral infection mainly attacks to children and older children. The viruses involved in this infection are parainfluenza virus, adenovirus, and respiratory syncytial virus. During this infection the patient have the barking cough. So this disease is otherwise known as barking cough and the medical term of croup is laryngotracheitis. The infection especially infects the larynx, subglottic tissue and trachea [1].

Literature review

Croup has all the characteristics of the common cold. It initiates with congestion, a stuffy or runny nose for a few days and may cause fever (over 101°F). The upper airway such as the lining of the trachea and larynx becomes progressively inflamed and swollen, so the larynx became narrow. The larynx goes into spasms, and the patient experiences difficulties in breathing. Also the patient feels harsh, loud, barking cough, hoarseness, tightness in the lungs. At this the mucus production may increases which block the airways. If the upper airway becomes swollen to the point where it is partially blocked off causes difficulties in breathing which leads to severe croup. At that time patient breathe very fast, and the stomach or the skin between the patient's ribs may seem to pull. Due to the lacking of oxygen a pale or blue color spots seen in the throat. [1].

The possible symptoms of the croup infection are a hoarse voice, barking cough, noisy breathing, fast breathing, runny and stuffy nose, fever. This infection lasts up to 5-6 days and generally severe at night time. This infection mainly attack to the children because of immature immune system and small size of air ways in bronchi.

There are 4 different types of croup

Laryngotracheobronchitis: The main causative agents are parainfluenza type 1 and 3, influenza A, adenovirus, respiratory syncytial virus, echovirus and mycoplasma. It affects mainly the children of ages between 3months to 5 years [2].

Spasmodic laryngitis (Spasmodic croup): It usually causes in children ages 1 to 3 years. It caused by an upper respiratory infection, allergy or psychological factors. Usually happens suddenly at night time [2].

Infectious laryngitis: it occurs in all people of all ages and is usually caused by a virus such as influenza, , rhinovirus or adenovirus. It may affect the vocal cord [2].

Epiglottitis: It causes in children of ages 2 to 6 years. This type of croup infections is very rare but sometime it is too serious. Hemophilus influenza type b is the main causative agent of it. The other types of croup involve in swelling of the windpipe, trachea and epiglottitis. The swollen epiglottis causes difficulties in breathing and if left untreated may lead to death by suffocation (lack of oxygen) [2].

Parainfluenza virus:

Parainfluenza belongs to the family Paramyxoviridae and of 5 subtypes such as 1, 2, 3, 4a, 4b. It is a single stranded RNA enveloped virus. It possesses fusion and hemagglutinin-neuraminidase glycoprotein spikes on their surface. It multiplies readily in primary monolayer tissue cultures. It mainly causes the upper respiratory disease such as croup, bronchiolitis or pneumonia [3].

Figure 8: parainfluenza virus particle