Med Micro Case Studies

Prior antibiotic treatment might increase the potential for infection with C. difficile by clearing out healthy, normal flora in the body, leaving room for the pathogenic bacteria to grow.

Fecal transplants can be used to treat C. difficile infections by introducing healthy flora/bacteria present on the stool from a healthy individual back into the body, thus clearing out the disease-causing bacteria and replacing it with normal flora

The thicker mucus observed in CF patients prevents cilial movement in the respiratory tract. The cilia are used to push harmful substances out of the body, but if their movement is inhibited, then they are unable to perform their function. This allows a buildup of various different pathogens in the mucus and respiratory tract.

Different Cl- concentrations in the lower respiratory tract could either increase or decrease susceptibility by making the environment more or less hospitable, or preventing pathogens from entering the body.

Increased levels of neutrophils in CF patients would seem to correlate to stronger immune responses, but the elevated presence of neutrophils in the blood can both block/inhibit airways and additionally cause immune-mediated damage to the respiratory tract.

P. aeruginosa may grow as normal flora in the GI tract because that is where it is supposed to be. In this environment, it would be non-pathogenic because it is not an abnormal growth, so the immune system would not attack it. Additionally, it is not producing any virulence factors, so no disease would be caused. However, if it gets somewhere it doesn’t belong - in this case, the respiratory tract - then it would likely shift to a pathogenic form and begin producing virulence factors, and the immune system will recognize it as a pathogen and mount an attack.

Neutropenia is characterized by a decreased number of neutrophils in the blood. Neutrophils are a part of the innate immune system. Therefore, a person with fewer neutrophils would be more susceptible to pathogens that reside in the blood (bacteremia, viremia, etc.)

Again, the complement system is a mechanism of the innate immune system. Someone who has deficient complement genes is more likely to be susceptible to recurrent infections.

A fever is a sign that the innate immune system has kicked into gear. Cytokines send signals to immune cells such as neutrophils, macrophages, & dendritic cells, which accumulate at the site of infection. The complement system also assembles, leading to the formation of the membrane attack complex (MAC). This localization of immune cells can cause inflammation. Additionally, and in the case of COVID, the body can regulate its temperature to make the environment inhospitable to invading bacteria. By in- creasing the temperature, there is a chance that the bacteria cells will die off.

The herpes virus is a double stranded DNA virus that is capable of integrating its genetic material into the genome of the host cell. NK cells are typically responsible for detecting infected cells that could potentially be tumorous. If an individual carries the genetic mutation for decreased or non-functional NK cells, then they have a greater disposition to developing tumorous and cancerous cells.

This tells us that NK cells play a critical role in helping to control herpes viruses in infected individuals by eliminating infected cells.

While the antibiotic killed off the bacteria, so it is no longer alive and able to reproduce, it did not eliminate the structures inside the body, which has spread to its entirety. The buildup of dead bacteria parts in the body, especially if they are gram negative, can act as an endotoxin, further sickening the patient.

dsDNA viruses such as influenza utilize eukaryotic cellular machinery to replicate their genetic material. Because they are located within a human cell, the innate immune system will not attack the virus because it recognizes the self. Additionally, many viruses have genes that destroy receptors that recognize pathogen-associated pattern receptors, which allow the virus to replicate without activating the immune system.

Women have two X chromosomes, meaning that they have two copies of certain genes which might code for and improve specific immune responses. Twice as many immune genes = strong immune responses.

Individuals lacking a spleen are more susceptible to certain bacterial blood infections because they are deficient in specific macrophages, which might play a role in preventing or fighting off different infections.

MHC II is involved with the antigen presenting cells (macrophages and dendritic cells) of the innate immune system, which then serve as the messengers to activate the adaptive immune response. The APCs opsonize exogenous pathogens and present the epitopes/antigens. CD4+ T cells bind to the epitope at receptor sites and can then relay the message on to other CD4+ T cells, allowing an adaptive immune response to develop. If an individual doesn’t have MHC II, then any pathogen that makes its way into the body will never have to face the adaptive immune system. Only the innate immune system is present to fight off the agent, and this usually will allow the infection to become chronic and permeate the body.

Decreased production of cytokines may prevent infected cells from sending out signals to attract immune cells to the site of infection. With this lack of initial immune response, neither the nucleated cells nor the antigen presenting cells of the innate immune response are specifically called to the infection site, so there are very few APCs to opsonize the fungus, present the antigens through MHC II, and initiate an adaptive response.

PAMPs are specifically designed to mimic patterns associated with certain pathogens. Adding them to the vaccine will amplify the pathogenic response, further activating the immune system into forming a response.

By killing off the CD4+ T cells and other immune cells, a person is left extremely susceptible to infection because they are lacking an adaptive immune response. This means that there is no fighting force for pathogens to go up against, so it is likely the agent will not be controlled or cleared.

HIV is capable of molecular mimicry, coating itself in host-cell-made sugar structures. This means the immune system either doesn’t recognize the virus, or won’t attack it to avoid harming self cells. It is also capable of shifting and/or hiding its epitopes to avoid immune detection.

CD8+ T cells are responsible for detecting epitopes presented on MHC I by the nucleated immune cells. This would pertain to cells infected by the measles virus. Without sufficient adaptive immune cells to eliminate infected cells, the measles virus is able to spread and eventually kill off the host.

IgA antibodies are usually found on the outside surface of various membranes. That means that while other antibodies are able to handle infections on the inside of the body, there is nothing to eliminate pathogens on outside surfaces before they establish an infection. This is especially true in the case of the respiratory tract, where pathogens can live on the outside surface of the throat/esophagus and cause infection.

This tells us that the infection is in the early stages, because IgM is the antibody associated with early infections, while IgG is associated with infections in their later stage.

The epitope for CMV viruses fuse to the Fc regions of IgG. NK cells and macrophages are triggered by the Fc regions of antibodies, so the macrophages opsonize the virus and present the epitope on their MHC I to activate the adaptive immune response.

Not everyone has the correct MHC I type to recognize specific epitopes.

The therapy might inadvertently attack host cells. Additionally, it is limited to specific epitopes and MHC dependent.

Donor cells, or from the bone marrow.

Vaccines can only be made if the body is capable of producing a natural immune response. Additionally, they can only be made if the pathogen exists within the blood, and if the body is able to clear the infection on its own.

Live-attenuated vaccines are very strong because they involve a live, albeit weakened, version of the pathogen. This elicits a strong immune response and good memory is formed. The disadvantages of live-attenuated vaccines are that, because it is a live pathogen, there is a risk of infection especially in individuals with weakened immune systems.

This is a passive immunization, meaning the response against it lasts only as long as antibodies are present.

Passive immunity does not build an adaptive immune response, as no self-made antibodies are made.

can get reinfections, especially since there are so many versions of the same virus. Also means that no vaccine can be made because of wide genetic diversity.

since no long-term memory response is formed, reinfections are possible. Also, it is not likely for a vaccine to be developed.

leads to potential for secondary bacterial infections, cannot develop a vaccine.

It is likely some type of bacterial exotoxin in the potato salad, meaning those who ate it were intoxicated with a large dose of the pathogen at once, causing disease.

Cold is a bacteriostatic agent, meaning it slows but does not eliminate bacterial growth.

Heat is a bactericidal agent, so it kills off the bacteria, helping to decontaminate infected foods.

Again, it is normal flora on the outside of our bodies, but when it gets inside the body, the conditions change and it may begin producing exotoxins, becoming pathogenic.

Because these are the same species with only slightly different genes, macroscopic, even microscopic, antigenic, and phenotypic tests will not work, you need to test using RFLP/PCR to distinguish between the two.

Transduction (bacterial “parasite” deposits genes from other bacteria), transformation (process of picking up genes from the environment), conjugation (acquisition of plasmids and other genes via sex pilus from one bacteria to another).

Transposition (genes moving within genome changes which genes are expressed.

Chlamydia is an example of an obligate intracellular pathogen meaning it can only replicate inside a host cell. These types of bacteria grow inside of host cells and do so by escaping lysosomes to avoid being broken down.

The lipopolysaccharide structures on the surface of all gram negative bacteria serve as endotoxins, so while the bacteria itself is not producing any toxins, the structures with enough accumulation can cause toxic shock and trigger the immune system into action.

Bacteria are capable of forming spores - stable, non-reproducing but hardy forms that can exist in the environment - and biofilms - multiple layers of the bacteria which makes it extremely difficult for antibiotics to penetrate and reach the original cell.

Ultimately, it is the exotoxin that is causing illness, and due to bacteria’s ability to acquire foreign DNA, other bacteria might be capable of producing an exotoxin associated with a different pathogen.

Fungal cells are very similar to our own in size and complexity. This makes it very difficult to develop antifungal drugs that will not end up harming our own cells. Usually, these medications target the cell wall that is found in fungal cells, but not human ones.

Antibiotic usage may clear out the normal flora that resides in the vagina, leaving room for a yeast to grow and cause an infection.

The immunocompromised or suppressed, who are unable to fight off fungal infections. Children, because there is less distance the fungus needs to travel to reach particularly vulnerable places and establish a systemic infection.

Wear a mask.

Mycoses can produce exotoxins as a result of their biochemical pathways, which are toxic to humans. If these exotoxins are present in the food, they can make you sick/cause hallucinations/kill you even without the fungus itself being present.

Black mold may cause illness under some conditions if the infected person has a compromised or suppressed immune system. Additionally, the amount of dimorphic fungi in the body can cause illness.

Fungi usually grow on sticks in the mold form. Sticks are pointy, which make them ideal objects for breaking the skin barrier and depositing a mold (which becomes a yeast) into the body.

Certain fungi are dimorphic, meaning they grow as molds in cold environments, typically outside of the body, but can transform into their yeast form when they are in warmer environments, such as the body.

This man has had years of exposure to yeast spores, which have likely established themselves in his digestive tract. These yeast ferment the sugar found in the food he eats, converting it to ethanol (alcohol) and causing a state of drunkenness.

Parasites are much larger, so to prevent them from entering the water, using a size filter would do the job. Some parasites are also resistant to chemical treatments.

Wear clothing, sleep under nets, or, in some cases, take drugs before arriving to help avoid or at least mitigate potential infections.

Getting contaminated water up the nose places parasites in the nasal cavity, with only a thin membrane separating it from the brain. If the parasite gets into the brain it causes infection there. Swallowing, on the other hand, takes the parasite down the esophagus into the stomach, a much longer distance for the parasite to travel to establish a brain infection.

Schistosomes cause a lot of immune mediated damage due to molecular mimicry. Using Praziquantel will likely end up targeting the few remaining immune cells in AIDS patients in addition to the parasite itself, worsening the current infection and all future infections. Additionally, antiparasitics work to unmask epitopes on parasites (usually are hidden), but once they are unmasked, there is no immune system to eliminate the parasite in AIDS patients.

Fecal-oral transmission. Animals such as cats (key carriers of toxoplasma gondii) may be natural reservoirs for certain parasites. If they defecate and humans come into contact with their feces, there is a chance for parasitic infections. Especially with sand, which might break the skin barrier through abrasion.

Parasites are capable of many different tactics to avoid immune responses such as antigen shifting or phase variation and masking epitopes to avoid immune detection.

Molecular mimicry.

The parasite expresses different genes depending on the signals it receives from the environment.

Many parasites rely on insect vectors for transmission. Indirectly, insecticides prevent certain parasitic infections by killing off the insect vector, so there is no way for the parasite to travel from host to host. Directly, some insects are the parasite, so insecticides would kill off the insect itself.

likely to be in the replicative form (e.g., trophozoite), cannot survive well in the environment due to poor protection

cyst, or environmentally stable form.

Acute and chronic infections to eliminate the virus. Systemic and localized.

Fights both chronic and acute infections, high efficacy of eliminating virus without causing harm to human cells. Targets stages of virus lifecycle.

Drugs do not clear viral infections; they are simply static agents designed to suppress viral replication. In patients with healthy immune systems, they might help the immune system control the virus, making it seem as though the drug is successful by minimizing disease. On the other hand, in those with suppressed or compromised immune systems, there is no immune system to control the virus even with the aid of the drug. Additionally, there are many different viruses that can cause the same disease, so there is a possibility that the antiviral drug being used is not the correct one for the virus.

Each antiviral drug is specific to one virus.

One protein can perform two different functions (Delivery and/or protection) but other viruses must produce two proteins: one to deliver, one to protect.

A virus might produce its spike/peplomer proteins last because these are the elements that go on the outermost surface of the cell. They are delivery proteins, so they need to be on the outside in order to find receptors to attach to.

Because they produce so much progeny.

The structural proteins can be used for vaccines.

They must be limited to humans and acute infections.

RNA is more prone to mutations than is DNA. Therefore there is a higher chance that an RNA virus might mutate in a way the codes for drug resistance.

Host cells do not have the primers or machinery needed to transcribe and translate viral RNA. With the exception of single stranded positive sense RNA viruses, all RNA viruses need to have RDRP (and for Retroviruses, DDDP) in order to replicate their genetic information.