The Complications Of Streptococcal Pharyngitis Biology Essay

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suppurative complications result from the spread of infection from the pharyngeal mucosa to deeper tissues by direct extension or by the hematogenous or lymphatic route and may include meningitis and pneumonia

meningitis is determined by high grade fever , neck rigidity, headache and photophobia

post streptococcal glomerulonephiritis is due to molecular mimicry between streptococcal antigen and basement membrane proteins of glomeruli as well as due antigen deposition in these membranes

it is determined by acute onset hematuria

acute rheumatic fever is also due to antigen mimicry in which antibody formed against streptococcal antigen cross react with valvular proteins of heart

it is determined with jones criteria 5 major criteria are migratory polyarthritis, pancarditis, subcutaneous nodules, erythema marginatum, and syndeham's chorea

Discuss the differences between food poisoning and gastroenteritis; be sure to include the effects of the form of the disease on the transmission, incubation period, the expected duration, and potential treatment. Name one organism that is associated with food poisoning, one organism that is associated with gastroenteritis, and one organism that is associated with both. (10 pts)

gastroenteritis is an cute infection characterised by sudden onset, nausea, vomiting, abdominal cramps, and diarrhea

transmission is through fecal-oral route.

incubation period depends on the causative agent but average incubation period is 1-3 days for most agents. However, The mean duration of EAEC-associated diarrhea cases in children under 3 years of age was 17 days, longer than that associated with any other pathogen.

this illness is expected to get relived within 2-8 days

treatment is mainly supportive and consists of manitainence of hydration and nutrition

main causative agents are viruses eg Human Caliciviruses. In addition, There are 5 different major strains of E. coli that cause gastroenteritis :Group 1 EPEC ,Group 2 ETEC ,Group 3 EHEC ,Group 4 EIEC ,Group 5 EAEC

food poisoning is bacterial infection usually caused by their toxins and acute in onset diarrhoea(may be associated with dysentry) , vomiting and fever

General symptoms include nausea, vomiting, diarrhea, abdominal cramping, discomfort, bloating, loss of appetite and fever

Can range from mild to severe

Most cases are self limiting and last no more than 24 hours

this bacterial infection is transmitted by infected food ingestion that contaminated with preformed toxins

incubation period is dependent on causative agent .for example, 1-6 hrs for staphylococcus aureus, 8-16 hrs for clostridium perfringens, and more then 16 hrs for vibrio cholrea

illness gets relived within 2 days for toxin producing bacteria and within 8 days for non toxin producing bacteria

treatment consists of oral rehydration solution and antibiotic agents

most common causative agents is Staphylococcus aureus 

Campylobacter jejuni  can cause food poisoning as well as gastroenteritis

Describe the pathogenesis of HIV infection from initial infection to the development of AIDS. Include how AIDs is defined and three potential agents of secondary infections associated with AIDS. (15 pts)

replication cycle of HIV begins with the high-affinity binding of the gp120 protein via a portion of its V1 region near the N terminus to its receptor on the host cell surface, the CD4 molecule on CD4 T helper cells

Once gp120 binds to CD4, the gp120 undergoes a conformational change that facilitates binding to one of a group of co-receptors

The two major co-receptors for HIV-1 are CCR5 and CXCR4. Both receptors belong to the family of seven-transmembrane-domain G protein-coupled cellular receptors, and the use of one or the other or both receptors by the virus for entry into the cell is an important determinant of the cellular tropism of the virus

Following binding of the envelope protein to the CD4 molecule associated with the above-mentioned conformational change in the viral envelope gp120, fusion with the host cell membrane occurs via the newly exposed gp41 molecule penetrating the plasma membrane of the target cell and then coiling upon itself to bring the virion and target cell together

Following fusion, the preintegration complex, composed of viral RNA and viral enzymes and surrounded by a capsid protein coat, is released into the cytoplasm of the target cell

As the preintegration complex traverses the cytoplasm to reach the nucleus , the viral reverse transcriptase enzyme catalyzes the reverse transcription of the genomic RNA into DNA, and the protein coat opens to release the resulting double-stranded HIV-DNA

At this point in the replication cycle, the viral genome is vulnerable to cellular factors that can block the progression of infection

With activation of the cell, the viral DNA accesses the nuclear pore and is exported from the cytoplasm to the nucleus, where it is integrated into the host cell chromosomes through the action of another virally encoded enzyme, integrase

HIV provirus (DNA) selectively integrates into the nuclear DNA preferentially within introns of active genes and regional hotspots. This provirus may remain transcriptionally inactive (latent) or it may manifest varying levels of gene expression, up to active production of virus.

some degree of activation of the host cell is required for the initiation of transcription of the integrated proviral DNA into either genomic RNA or mRNA

Following transcription, HIV mRNA is translated into proteins that undergo modification through glycosylation, myristylation, phosphorylation, and cleavage

The viral particle is formed by the assembly of HIV proteins, enzymes, and genomic RNA at the plasma membrane of the cells

Budding of the progeny virion occurs through specialized regions in the lipid bilayer of the host cell membrane known as lipid rafts, where the core acquires its external envelope

any HIV-infected individual with a CD4+ T cell count of <200/L has AIDS by definition, regardless of the presence of symptoms or opportunistic diseases

3 infections which can cause secondary infections in AIDS patient are candida, Mycobacterium avium complex, Pneumocystis jiroveci

Compare and contrast the cholera toxin and the pertussis toxin. Describe the target cell of each, how the toxin effects the target cell, what the effect of the toxin on that target cell is, and the role of the toxin in the pathogenesis of the organism (i.e. what signs and symptoms of the disease are associated with the toxin). (10 pts)

Cholera toxin is a proteinaceous toxin with 2 subunits. Cholera toxin cannot be toxoided

Cholera toxin is made up of t subunits A and B, B subunits bids with the Gm1 ganglioside recptor on intestinal epithelial cell. A subunit is broken down intoA1 and A2. A2 links subunit A1 and B. A1 then stimulates adenl cyclase which synthesizes cAMP which leads to increased secretion of water and electrolytes into the intestinal lumen

Pertusis toxin is also a proteinaceous toxin which is haet labile and major virulence producing factor. It can be toxoided and hence its vaccine can be produced

Pertusis toxin is made up of 2 subunits A and B, where B is the binding component and A acts as the lymphocytosis producing , histamine releasing and islet activating factor

Target cell of cholera toxin is the intestinal epithelial cell

Target cells of the pertusis toxin are the mast cells , lymphocytes, and the islet cells

Cholera toxin is the only mainstay of vibrio infection. It responsible for all the symptoms of the choleara infection

Cholera toxin leads to secretory diarrohea and rice water stool production as well as mucus flakes in the stools

Pertusis toxin one of the several virulence factors of bordetella pertusis infection. It responsible of significant no. Of the symptoms of whooping cough disease

Pertusis toxin causes hypoglycemia, lymphocytosis and erythema and hypotension

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Pertusis toxin

Compare and contrast pulmonary anthrax and pneumonic plague. Indicate the cause of each, where the two are found globally (generally-don't need specific regions of the world), how each is transmitted, what the major signs and symptoms are, and how each is resolved. Speculate on why pneumonic plague been associated with history-changing epidemics, while pulmonary anthrax is observed only rarely. (12 pts)

Anthrax infection begins on average 10 days after exposure with fever, malaise, headache, dyspnea, cough, and congestion of the nose, throat, and larynx. Within hours to a few days, progression to the fulminant stage of infection occurs in which symptoms or signs of overwhelming sepsis predominate. Delirium, obtundation, or findings of meningeal irritation suggest an accompanying hemorrhagic meningitis.

Causative agent is the inhaled spores of bacillus anthracis

It came into notice with association post 9/11 anthrax attacks through the U.S. Postal System. So till now its max cases are seen only in USA

It is transmitted through inhalation , ingestion of direct prolonged skin contact with the spores

ciprofloxacin is considered the drug of choice for treatment and for prophylaxis following exposure to anthrax spores. The prognosis in cutaneous infection is excellent

Plague is an infection of wild rodents with Yersinia pestis, a small bipolar-staining gram-negative rod

The onset is sudden, with high fever, malaise, tachycardia, intense headache, delirium, and severe myalgias. The patient appears profoundly ill. If pneumonia develops, tachypnea, productive cough, blood-tinged sputum, and cyanosis also occur. There may be signs of meningitis. Pustule at the site of inoculation may be present

It is endemic in north American states (CA, UT, AZ, NV, NM, CO).

It is transmitted among rodents and to humans by the bites of fleas or from contact with infected animals. Following a fleabite, the organisms spread through the lymphatics to the lymph nodes, which become greatly enlarged. They may then reach the bloodstream to involve all organs

Streptomycin , gentamicin and doxycycline are effective against it

Plague spreads via rodents and droplets of the infected individuals. Also it has a short incubation period. Thus rodents being ubiquitus in there presence i.e. present through out the globe and then rapid spread of the infection from the infected person contribute to the epideminogeinc potential of plague

Flea control and personal hygiene help to prevent plague

Whereas anthrax is spread only through direct infection from the spore and is not transmitted by the infected patients hence its widespread epidemics are not known

Describe infectivity cycle of HIV for a cell, including the attachment, entry, synthesis, maturation and release. Identify all the components that are packaged within the virion and discuss the role of all important factors including gp41, gp120, tRNAlys, integrase, protease, and reverse transcriptase. Indicate at least three steps at which current anti-HIV drugs act. What is one mechanism by which HIV avoids exposure to the immune system-particularly humoral immunity, and what factor allows that to happen? (15 pts)

replication cycle of HIV begins with the high-affinity binding of the gp120 protein via a portion of its V1 region near the N terminus to its receptor on the host cell surface, the CD4 molecule on CD4 T helper cells. Once gp120 binds to CD4, the gp120 undergoes a conformational change that facilitates binding to one of a group of co-receptors

The two major co-receptors for HIV-1 are CCR5 and CXCR4.

Following binding of the envelope protein to the CD4 molecule associated with the above-mentioned conformational change in the viral envelope gp120, fusion with the host cell membrane occurs via the newly exposed gp41 molecule penetrating the plasma membrane of the target cell and then coiling upon itself to bring the virion and target cell together

Following fusion, the preintegration complex, composed of viral RNA and viral enzymes and surrounded by a capsid protein coat, is released into the cytoplasm of the target cell

As the preintegration complex traverses the cytoplasm to reach the nucleus , the viral reverse transcriptase enzyme catalyzes the reverse transcription of the genomic RNA into DNA, and the protein coat opens to release the resulting double-stranded HIV-DNA

With activation of the cell, the viral DNA accesses the nuclear pore and is exported from the cytoplasm to the nucleus, where it is integrated into the host cell chromosomes through the action of another virally encoded enzyme, integrase

HIV provirus (DNA) selectively integrates into the nuclear DNA preferentially within introns of active genes and regional hotspots. This provirus may remain transcriptionally inactive (latent) or it may manifest varying levels of gene expression, up to active production of virus.

The viral particle is formed by the assembly of HIV proteins, enzymes, and genomic RNA at the plasma membrane of the cells

Budding of the progeny virion occurs through specialized regions in the lipid bilayer of the host cell membrane known as lipid rafts, where the core acquires its external envelope

Components that are packaged within the virion are gp120, gp41, genomic RNA, enzyme reverse transcriptase, p18(17) inner membrane (matrix), and p24 core protein (capsid)

Role gp41 acts as an transmembrane anchor in the phospholipid bilayer. Gp 120 act as receptor for binding withCD4 ligand over the T helper cell, reverse transcriptase helps to form DNA copies of the RNA genome of the virus to integrate with the host genome, integrase causes ligation of the HIV's DNA with the host DNA, protease helps in synthesis and integaration of the viron bodies during replication, cellular tRNAlys is the key component of the viral nucleocapsid which helps in the translation of the mRNA to the capsid Protiens of the viron

Mechanism of action of NRTI (eg Zidovudine) it blocks the synthesis of DNA from RNA of the virus by blocking the action of reverse transcriptase inhibitor

Enfuvirtide is a new drug which inhibits the fusion of the viral genome to the t helper cell

Protease inhibitor (eg saquinavir) blocks the assembly of the viral particles while release of the newly formed virons

One of the principal mechanisms of immune escape is the addition of N-linked glycosylation sites. The added carbohydrate moieties interfere with envelope recognition by these initial antibodies. The hyperglycosylation of the envelope protein has been termed the glycan shield

HIV escapes cellular immunity by directly infecting the CD4 t helper cells which are the mainstay for activation of rest of the pathways

Both hookworms and pinworms are intestinal helminths. Explain how each is acquired by the host and in what stage of the worm's life cycle. Auto (or self) infection occurs for one, but not the other. For which one can self-infection occur? How does self-infection for that particular agent occur? Why can self-infection occur for one, but not the other? Your answer for the last question should consider the stage of the infectious agent required for infection, the route of transmission and the development of the agent within the host. (8 pts)

Infection of hookworm is acquired when infectious filariform larvae penetrates the skin bare skin of the foot

Stage of the infection of the hookworm is its second larval stage i.e. filariform larva

Pinworm or Enterobiasis is transmitted person-to-person via ingestion of eggs which may contaminate fomites , food, or hands

Stage of infection in humans of pinworn is the egg stage

Autoinoculation occurs only for Pinworm or Enterobiasis

Female pinworm mature in about a month, and remain viable for about another month. During this time they migrate through the anus to deposit large numbers of eggs on the perianal skin. There these eggs cause itching and these eggs get inoculated into the fingers of the child leading to autoinoculation

Autoinoculation occurs only on case of pinworm and not hookworm because pinworm's lifecycle is independent of requirement of external factors like in case of hookworm it requires conversion of egg into rhabditiform larvae also soil is the site for filariform larvae

Another reason for autoinoculation in case of pinworm is that route of primary infection is mouth which is handled a lot making it a prone site but in case of hookworm site of portal entry is skin invasion which cannot be site for autoinoculation

Give three potential reasons why developing an HIV-vaccine is so problematic. Explain why these aspects of HIV make vaccine development unlikely (at least currently). (8 pts)

HIV is a retrovirus which consists of RNA genome . now RNA lacks histone proteins this contributes to the unstability of the genome and makes it susceptible to frequent mutations and hence frequent change in the antigenic structure. This change in antigenic structure makes the antibodies against previous antigens ineffective hence vaccine is not of use

HIV's mechanism of replication consists of enzyme reverse transcriptase which which has no proof reading mechanism and this makes it more mutable during the replication stages again contributing to the variation in the antigenic structure.

Also added carbohydrate moieties to the surface antigen interfere with envelope recognition by these antibodies that are formed in response to the vaccine

Also as for now it has not been possible to attenuate the prototype virus for HIV as the virus has high affinity to get mutated into the wild virulent strain

Also most clinical trial which have happened till now have been directed against preventing disease and not the infection . this will never eliminate the virus from the body and any mutation will cause remission of the disease

Also of all the vaccines tried till now neither the killed nor the attenuated viruses have retained their antigenicity which may lead to vaccine failure

Of all the vaccines tried till now the immunity is only against blood infection but it has no protective value against the most common route of infection i.e. genital route where it provides no secretion of antibodies

Also HIV isolates are themselves highly variable HIV can be categorized into multiple clades and subtypes with high degree of genetic divergence. Therefore the immune response generated by any vaccine need to be broad enough to account for this variability. Any vaccine that lacks this breadth is unlikely to be effective. These are the main reasons that vaccine against HIV is highly unlikely in immediate future

We described a number of cellular (non-viral) organisms, like the relapsing fever spirochetes, Neisseria gonorrhoeae, and the Trypanasoma species, that have the ability to change their surface proteins during the course of an infection. Draw a diagram that demonstrates at the molecular level how this change occurs.

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Spirochetes have upto five variants inside the human host for vlsE protein

Spirochete also have two different variants for Osp antigen

This variation in the antigenic structure of spirochetes leads to four possible combinations in Osp protein and numerous antigenic variants combinations for vlsE antigen

So at a single time human immune system is receiving over 100 of variants of single bacteria making it near impossible for it to cover up all the antigens

Each time when it suppress these antigens it leads to shifting of the antigenic combination to those combinations against which antibodies were not formed

Spirochetes have more time to alter their surface proteins towards the end of the tick's feeding bout making it important to have the tick removed as early as possible

Also with the bite of the tick, its salivary proteins are also injected into the human blood and these antibodies are suppressive to the immune system.

Also it has been seen that there is temperature dependent variation in the antigenic structure of the spirochete particularly inside the tick

Tolerance mechanism is also attributed towards this decreased susceptibility of the bacteria to the antibodies. Tolerance is not suppressed immune system it is just decreased specificity of the anti gens to the antibodies

A spirochete surface protein uncouples store operated calcium channel in fibroblasts . this a mechanism particularly active against cytotoxic T cell immune system

A new surface protein vtp which was previously thought to be existing in single form has now been described in 31 types thus further adding to the variability in the antigenic structure of the spirochete

Horizontal gene transfer among gene of 16s RNA, flab, gyrB, and glpQ along with recombination within and between two genomic groups were responsible for the variation observed in the antigenic structure

with assignment Q no

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