Pathogen in a broad sense is anything that can infect and can cause a disease. It is a type of infectious agent that can be a virus, bacteria, prion, fungus, viroid or parasite that causes diseases in the host and the host can be a fungus, a plant, an animal or any microorganism also. Soon after the recognition and entry into the host cells, the damaged cell of the host disintegrates; the virus-lacking envelope is released rapidly. Viruses with an envelope are released slowly without immediate disintegration of the host cell. Apart from being released slowly or rapidly there is a possibility where viruses become long term residents of the host. Example: Herpes simplex virus that follows such possibility and causes fever and blisters. In animal Herpes virus infects and damages the epithelial tissues; it then spreads to the nerve cells and become inactive. During this period, it resides in nerves near the skin. They get reactivated by the emotional or physical stress, chemical or microbial infections. They damage the epithelial cells of the skin upon reactivation. After the usual childhood case of chicken pox, the virus remains inactive in person‘s nerve cells, if anytime reactivated it causes painful skin condition called shingles. Retrovirus One defining characteristic of retrovirus is the use of viral reverse transcriptase. Retroviruses carry this enzyme in their genome and use it and convert its single stranded RNA into a double stranded DNA. Other viruses use the host cell’s polymerase enzymes.
A key feature of the retrovirus reverse transcriptase is the lack of a proofreading ability, an ability that is found in cellular polymerase enzymes. This lack of proofreading increases the number of errors while the virus converts its RNA to DNA. Errors in this transcription process result in slightly different genetic codes or mutants.
Once the virus has successfully gained entry into the host cell, the endosome acidifies, which alters the virus topology by causing capsid components to disassociate. These changes as well as the toxic nature of the pentons of their structure results in the release of virion into the cytoplasm. With the help of cellular microtubules, the virus is transported to the nuclear pore complex, whereby the adenovirus particle disassembles. Viral DNA is then subsequently released, which can enter the nucleus via the nuclear pore.
The DNA then associates with histone molecules. Thus, viral gene expression can occur and new virus particles can be generated. DNA replication process divides adenovirus life cycle into two phases: an early and a late phase. In both phases, a primary transcript, i.e., alternatively spliced to generate monocistronic mRNAs compatible with the host‘s ribosome is generated, allowing for the products to be translated.
There are four stages to the adenovirus replication cycle
- First the cell binds to surface receptors on the target cell and enter the cell via endocytosis.
- The virion then sheds its endosome coat and enters into the nucleus.
- In the nucleus the virion releases its genes, which are then read by the machinery inside of the host cell.
- The adenovirus has both early and late genes.
The early genes code for non-structural, regulatory proteins, while the late genes code for replication substrates and machinery.
After transcription, these genes are translated, the new progeny are assembled and then they exit through cell lysis.
Responses Elicited by Disease
Cell wall reinforcement (callose, lignin, suberin, cell wall proteins).
Antimicrobial chemicals and proteins.
Hypersensitive response: a rapid host cell death response associated with defense mediated by resistance genes.
Endophyte assistance from plant roots: the release of chemicals that attracts beneficial bacteria to fight against infections. In plants Tobacco Mosaic Virus (TMV) it is very stable. The viral RNA is infectious by itself, but the addition of a protein coat protects the RNA from enzymes that would destroy it. The protein coat poses a problem, that it must be removed once the virus gets inside a cell. TMV uses two tricks to release its RNA. As with many viruses, TMV has chemicals that cause the protein to change when the environment changes. The capsid protein has several clusters of acidic amino acids that are stable outside of cells, where calcium levels are high, but repel each other in the low-calcium conditions inside the cell. This is to loosen the first few capsid proteins, releasing the end of the RNA. TMV then uses ribosomes as the supporter to finish the process. As the ribosomes move down the strand, creating the first set of virus proteins, they displace the remaining capsid proteins. If the RNA and capsid proteins are mixed together, they spontaneously form functional viruses.
A two-step process is used for their assembly.
- First, the TMV protein forms a two-layer disk, with 17 proteins in each ring. A special initiation sequence in the RNA then binds in the hole at the center. This causes the disk to dislocate, forming a ring shaped with 16 +1/3 subunits per turn.
- The remaining subunits then stack on this structure, elongating until the RNA is covered. There is a great advantage to this two-step process: the need for an initiation sequence in the RNA ensures that only virus RNA is packaged into viruses.
Diseases caused by pathogens
Trypanosoma gambience are the causative organism for the African sleeping sickness. Different species of the trypanosoma family namely T.rhodosiense and T.cruzi cause the sleeping sickness. Gambiensis reside in blood, lymph and cerebrospinal fluid. Three main hosts for gambiensis are
- Definitive host- Man
- Intermediate host- Tse-Tse fly or Glossina palpalis, Glossina tachynoides.
- Reservoir host- Antelopes, Pigs and Buffaloes.
Parasite reproduces by longitudinal binary fission. They respire anaerobic and excrete by diffusion. Trypomastigote form of Trypanosoma present in human blood enters the Fly‘s stomach and multiplies by binary fission. There are three forms namely stumpy, intermediate and slender.
During first stage, parasite resides in blood but no significant symptoms appear. After an incubation period of 6-10 days, the parasite enters the lymph nodes and multiplies in cells of lymph glands and causes swelling. There is an increase in number of WBCs and enlargement of liver and spleen. The symptoms include nausea, headache, unconsciousness and irregular fever.
Morphology of the malaria parasite Plasmodium falciparum inside the infected erythrocyte
Early trophozoite (double infection).
Early trophozoite double chromatin with a few Maurer’s dots.
Late trophozoite with Maurer’s dots and crenated red cell.
Mature schizont with merozoites and clumped pigment.
Macrogametocyte with bluish cytoplasm and compact chromatin.
Microgametocyte with pinkish cytoplasm and dispersed chromatin.
It is also known as whooping cough, a highly contagious disease caused by the bacterium Bordetella pertussis.
After two-day incubation period, pertussis in infants and young children are characterized initially by mild respiratory infection symptoms such as coughing, sneezing and runny nose (catarrhal stage). After one to two weeks, the cough changes character, with an increase of coughing followed by an inspiratory whoop‘ sound (paroxysmal stage). Coughing fits may be followed by vomiting due to the sheer violence of the fit. In severe cases, the vomiting induced by coughing fits can lead to malnutrition and dehydration. The fits that do not occur on their own can also be triggered by yawning, stretching, laughing or yelling. Triggering fits gradually diminish over one to two months during the convalescent stage. Other complications of the disease include pneumonia, encephalitis, pulmonary hypertension and secondary bacterial super-infection.
Adults and adolescents are the primary reservoirs for pertussis. It is spread by contact with airborne discharges from the mucous membranes of infected people, who are most contagious during the catarrhal stage. Because the symptom during the catarrhal stage is non-specific, pertussis is usually not diagnosed until the appearance of the characteristic cough of the paroxysmal stage.