I.

INTRODUCTION OF THE CASE

Name: Victorino “Mang Vic” Magtanggol

Age: 75 years old
Sex: Male

Mang Vic, a fisherman, rushed to the hospital this morning for chest pain and chills.
Upon arrival, he coughed with blood.

Story time prior to check up:

He started smoking at the age of 14 until now. He can consume 100 sticks of cigarettes
per day. According to him, last week they celebrated their fiesta and Mang Vic with his friend,
Mang Canor, had their tagay session. Four (4) days after their fiesta, Mang Canor was
diagnosed and confirmed to be COVID positive. Mang Vic already had an on and off cough.
However, he thought it was just due to the changing weather. Three (3) days after Mang Canor
was diagnosed with COVID, Mang Vic was experiencing chest pain and chills. So he was
rushed to the hospital.

BMI: Underweight
Chest PA:
Trachea is midline
Heart shadow is not enlarged
Intact both diaphragm and costophrenic angles and
other chest structures are normal however,
Reticulo-Fibroid infiltrates are seen in the upper lungs

Mang Vic underwent sputum, covid, and tuberculin skin test. What do you think is the
diagnosis? Justify your answer.
~~~~~~~~~~ START OF JULIA’S PART
II. TUBERCULOSIS
About 2 billion people worldwide are infected with Tuberculosis (TB). That is a lot of
people but 90-95% are not aware that they are infected. This is because our immune system
works disallowing Tuberculosis to multiply.
The Philippines ranks fourth worldwide in tuberculosis incidence. About 1
million Filipinos have active tuberculosis, and nearly 70 Filipinos die every day from this curable
disease. And for every 100,000 Filipinos, an estimated 650 individuals were infected with TB in
2021.

A. Bacterial Agent: Mycobacterium Tuberculosis

1. Type of Bacteria
The pathogen that causes this disease is a bacterium called Mycobacterium
tuberculosis (M. tuberculosis). This bacterium is rod-shaped and needs oxygen to survive. Its
cell wall has mycolic acid which stains red as seen under the microscope. The wall is incredibly
hardy making it resistant to weak disinfectants and can survive on dry surfaces for months.
2. Transmission (when and where)
M. tuberculosis is carried in airborne particles, called droplet nuclei, of 1–5 microns in
diameter. Infectious droplet nuclei are generated when persons who have pulmonary or
laryngeal TB disease cough, sneeze, shout, or sing. Depending on the environment, these tiny
particles can remain suspended in the air for several hours. However, M. tuberculosis is
transmitted through the air, not by surface contact. Transmission occurs when a person inhales
droplet nuclei containing M. tuberculosis, and the droplet nuclei gain entry in the respiratory
tract. It can traverse the mouth or nasal passages, pharynx, larynx, trachea, and bronchi to
reach the alveoli of the lungs. Several factors determine the probability of transmission of M.
Tuberculosis.

B. Pathophysiology of Tuberculosis
1. Primary Tuberculosis
But we actually breathe in all sorts of viruses and bacteria all the time, but the body have
defenses against these. Like mucus in the trachea which can trap the bacteria and expel it from
the body. But smaller TB droplets can make their way to the lungs down to the alveoli where we
have macrophages that eat up foreign materials and destroy them. It does this when a
macrophage recognizes the foreign proteins of the bacterium. This is now called a phagosome
because it has a lysosome that has hydrolytic enzymes that will break down any biochemical
molecule. But TB is tricky because once it is inside the macrophage, it releases proteins that
inhibit the lysosome so it cannot be destroyed. The bacteria lives and it proliferates creating a
localized infection. At this point, the person now has primary tuberculosis. This means that
they have signs of infection after exposure. Most people at this stage are asymptomatic or have
mild flu-like symptoms.
Three weeks after initial infection, cell-mediated immunity kicks in. Immune cells
stimulated by cytokines surround the site of infection creating a granuloma to wall off bacteria to
keep it from spreading. The tissue inside dies as a result, a process called caseous necrosis
which means cheese-like necrosis. This area is called ghon focus. This usually forms in the
middle and lower lobes of the lungs and it is subpleural. Sometimes these ghon focus migrate to
the nearby lymph nodes causing granulomas in the lymph nodes, the hilar lymph nodes grow
bigger causing hilar lymphadenopathy. The combination of ghon focus and hilar
lymphadenopathy make up the characteristic ghon complex of TB. The complex undergoes
fibrosis and often calcification producing a scar tissue seen on the xray: *insert xray pic* The
calcified ghon complex is called the Ranke complex. The ranke complex is a characteristic
consistent with Primary TB.
In some cases, TB is killed off. But in other cases, usually greater than or equal to 90%,
TB remains viable and is therefore alive but goes dormant, called the latent phase, which will
be discussed by my other groupmate. In 10% of the cases, primary tuberculosis progresses to
primary progressive tuberculosis, usually if the immune system is compromised. The ghon
focus can spread to one or both upper lobes of the lungs because this is where oxygenation is
greatest and again, mycobacterium tuberculosis loves and needs oxygen.
The memory T cells again release cytokines and repeats the process earlier resulting to
more caseous necrosis. This time the caseous necrosis tends to cavitate or form cavities which
allows bacteria to escape and disseminate to other areas other than the lungs. It can cavitate
and extend to the edge of the lungs destroying some of the tissues of the parenchyma and into
the pleura, air will leave and go out to the pleural space resulting to pneumothorax. These
necrotic tissue still spread throughout the lungs and cause more pus and fluid accumulation
leading to bronchopneumonia. Massive amounts of cytokines and more inflammatory reaction
to the lungs will cause increased capillary permeability so fluid can accumulate in the pleural
leading to pleural effusion, which is why TB pleurisy is a common finding. Pneumothorax,
bronchopneumonia, and pleural effusion are the clinical signs but usually the patient will
complain of pulmonary symptoms. The fibrocavitary lesions that are necrotic eats the lung
tissue, when it does, it will also eat the blood vessels around it so the patient will start coughing
up blood, a symptom called hemoptysis. Also, the fibrocavitary lesions will increase and can
compress the bronchopulmonary areas, the structures cannot clear secretions so there will be
hyperinflammation of these structures and will lead to productive cough. As airways are
inflamed, cough receptors can trigger cough reflex so patients will also present with cough,
often productive cough.
Again, many cytokines will be released, these cytokines also stimulate the hypothalamus
which controls our appetite and temperature so patients with TB can also present with fever,
night sweats, and weight loss.
As I have mentioned, 90% of cases of TB go into the latent phase and it can be
reactivated when the individual’s immune function is compromised. Reactivated TB will now be
discussed by Jed.
—-------------—-----JEDWYNNNNNNNNNNNNNN<3—----------------------------------------

2. Reactivation TB / Post Primary TB

Reactivation TB may occur if the individual's immune system becomes weakened and
no longer is able to control the bacteria. The bacteria then overwhelm the immune process and
make the person sick with TB.
The greatest risk for developing reactivation TB disease is within the first two years
following the initial infection as a contact to a person with infectious TB.
 Reactivation can also occur more readily in people with HIV, diabetes mellitus,
malnutrition, or those who take medications that weaken the immune system, such as
medications for rheumatoid arthritis, steroids, or cancer chemotherapy. It can also occur with
aging and weakening of the immune system. Reactivation may also occur for other unknown
reasons.
a. Differentiate from Primary TB
Primary tuberculosis and reactivated tuberculosis are both forms of tuberculosis
(TB). However, they differ in terms of the timing of their onset and the course of the
disease. Primary tuberculosis occurs when a person is first exposed to the M.
tuberculosis bacteria and develops an initial infection. In some cases, the body's immune
system is able to control the infection, and the bacteria become dormant. This is known
as latent TB infection.
Reactivated tuberculosis, also known as post-primary or secondary TB, occurs
when the M. tuberculosis bacteria that have been dormant in the body become active
again.

3. Extrapulmonary Tuberculosis
Tuberculosis (TB) can spread from the lungs to other parts of the body, which is known
as extrapulmonary TB. Some of the common complications of TB in other parts of the body
include:
 Tuberculosis of the lymph nodes: This is the most common form of
extrapulmonary TB. The lymph nodes in the neck, armpits, or groin can become
swollen and painful.

 Tuberculosis of the bones and joints: TB can affect the bones and joints, causing
pain, swelling, and stiffness. The spine is the most commonly affected site, leading to
a condition called Pott's disease.

(CT and MR of spine tuberculosis. A. CT of spine TB: anterioposterior position;

B. CT of spine TB: lateral position; C. MR of spine TB)
 Tuberculosis of the urinary tract: TB can cause inflammation and damage to the
kidneys and bladder, leading to symptoms such as pain during urination, blood in the
urine, and frequent urination.

 Tuberculosis of the central nervous system: TB can affect the brain and spinal
cord, leading to symptoms such as headache, confusion, seizures, and difficulty with
coordination.

 Tuberculosis of the gastrointestinal tract: TB can affect the intestines, leading

to symptoms such as abdominal pain, diarrhea, and weight loss.

 Tuberculosis of the skin: TB can cause skin lesions and ulcers, which may be
painful or itchy.
 In summary, TB can affect various parts of the body, leading to a range of complications.

C. Symptoms
The symptoms of TB can vary depending on the stage of the infection and the part of the
body that is affected. In the early stages, there may be no symptoms or only mild symptoms
such as a persistent cough, fatigue, and weight loss. As the infection progresses, the following
symptoms may develop:
1. Coughing up blood or sputum
2. Chest pain
3. Fever and night sweats
4. Loss of appetite
5. Fatigue
6. Shortness of breath
7. Swelling of lymph nodes, particularly in the neck
The processes involved in the development of these symptoms were discussed earlier in
the pathophysiology section.

D. Diagnosis and Treatment

Diagnosis of tuberculosis (TB) typically involves a combination of medical history,
physical examination, and laboratory tests. The following are some of the common methods
used to diagnose TB:
1. Tuberculin skin test: A small amount of purified protein derivative (PPD) is injected
under the skin of the forearm. The test measures the body's immune response to the TB
bacteria.

2. Chest X-ray: A chest X-ray can show any abnormalities in the lungs, such as cavities
or infiltrates, that may be caused by TB.
 3. Sputum culture: A sample of sputum (mucus coughed up from the lungs) is collected
and analyzed in a laboratory to detect the presence of the TB bacteria.

4. Molecular tests: These tests use DNA or RNA analysis to detect the TB bacteria in
sputum or other samples.

Once TB is diagnosed, treatment usually involves a combination of antibiotics taken for

several months. The most common antibiotics used to treat TB include isoniazid, rifampin,
ethambutol, and pyrazinamide. The exact combination of antibiotics used and the length of
treatment depend on the severity of the disease and other factors such as the patient's age,
medical history, and drug resistance.
It is important to take all of the prescribed antibiotics as directed, even if the symptoms
improve, to prevent drug resistance and ensure complete eradication of the bacteria.
Recent studies suggest that human stem cells may serve as a protective niche for
dormant Mtb having reactivation potential. Mesenchymal stem cells may also achieve the
purpose of treating TB by regulating the inflammatory response of TB, alleviating the lung injury
of TB, affecting the survival of host cells and clearing bacteria.

—-------------—-----JEDWYNNNNNNNNNNN <3—----------------------------------------
---------Start of Nina Maganda’s part-----------------
III. COVID19
On March 11, 2020 the World Health Organization declared a pandemic because the
rapidly spreading because of the corona virus 19 disease or simply put, COVID19. But, what is
COVID 19?
Definition:
Covid19 is a novel coronavirus belonging to the family Coronaviridae, and was named
as the severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2). It was seen to be
highly homologous to the SARS coronavirus (SARS-CoV), which was responsible for the
respiratory pandemic during the 2002–2003 period. The respiratory illness caused by this virus
was termed as coronavirus disease 2019 or simply COVID-19 by the WHO, and the outbreak
was considered to have started via a zoonotic spread from the seafood markets in Wuhan,
China
A. Pathogen: Coronavirus
1. Type of virus
Viral Life Cycle:
Coronaviruses are made up of four structural proteins, namely, the spike (S), membrane
(M), envelop (E) and nucleocapsid (N) proteins. The S protein is the most important for
attachment and penetration of the host because it protrudes from the viral surface.
Host Cell Invasion:
 Virus binds to host receptors
 Enters host through endocytosis or membrane infusion
 After membrane fusion, virus enters pulmonary epithelial cells and releases viral
contents
 Virus undergoes replication and formation of negative strand RNA
 Negative strand RNA produces new positive strand RNA
 The viral N protein binds the new genomic RNA and the M protein facilitates
integration
 Newly formed Nucleocapsids are then enclosed in the ER
 The new viral particles are now ready to invade the adjacent epithelial cells as well
as for providing fresh infective material for community transmission via respiratory
droplets
 Figure: The severe acute respiratory syndrome coronavirus-2 life cycle.
2. Transmission:
Based on studies and recent publications by the World Health Organization, the
COVID19 virus is transmitted via droplets, airborne (aerosol), contaminated surfaces, other
fluids and contact with the infected.
Transmission of respiratory infections are transmitted via droplets of different sizes:
 >5-10 um referred to as respiratory droplets
 <5 um in diameter referred to as droplet nuclei
occurs when a person is in in close contact (within 1 m) with someone who has
respiratory symptoms (e.g., coughing or sneezing) and is therefore at risk of having his/her
mucosae (mouth and nose) or conjunctiva (eyes) exposed to potentially infective respiratory
droplets. Transmission may also occur through fomites in the immediate environment around
the infected person.
Airborne (aerosol) transmission:
refers to the presence of microbes within droplet nuclei and can remain in the air for long
periods of time and be transmitted to others over distances greater than 1 m. Airborne
transmission may be possible in specific circumstances and settings in which procedures or
support treatments that generate aerosols are performed:
 endotracheal intubation,
 bronchoscopy,
 open suctioning,
 administration of nebulized treatment,
 manual ventilation before intubation,
 turning the patient to the prone position,
 disconnecting the patient from the ventilator,
 non-invasive positive-pressure ventilation,
 tracheostomy, and
 cardiopulmonary resuscitation.
Other fluid transmission:
Via: feces, saliva, urine, semen, and tears
Contact with the infected:
 Through direct contact with someone who has the virus
 Mother to child
- Rare but not absent
- Newborns may also be infected post-delivery via breastfeeding or via inhalation
of droplets produced by infected parents and/or healthcare professionals.

—---END OF NINA MAGANDA’S PART—-------

—--HERNEL—-------------------------------------------

B. Pathophysiology of COVID19
1. Asymptomatic phase
 SARS-CoV-2 enters the body through respiratory aerosols and binds to nasal epithelial
cells in the upper respiratory tract. The ACE-2 receptor is the primary host receptor for viral
entrance into cells, and it is found to be abundantly expressed in adult nasal epithelial cells. The
virus replicates and spreads locally, infecting ciliated cells in the conducting airways. This stage
lasts a few days and produces only a minimal immunological response. Despite having a low
viral load, the individuals are highly contagious, and the virus can be diagnosed through nasal
swab testing.
2. Invasion of Upper & Lower Respiratory Tract
The virus migrates from the nasal epithelium to the upper respiratory tract via the
conducting airways at this stage. The disease shows up as fever, fatigue, and dry cough due to
the involvement of the upper airways. During this phase, there is a stronger immunological
response involving the release of C-X-C motif chemokine ligand 10 (CXCL-10) and
interferons (IFN- and IFN-) from virus-infected cells. Most patients fail to progress beyond this
stage because the established immune response is sufficient to keep the virus from spreading.
Invasion of the lower respiratory tract, approximately one-fifth of all infected patients
proceed to this stage and acquire severe symptoms. The virus infiltrates and enters type 2
alveolar epithelial cells via the host receptor ACE-2, where it begins replicating to make new
viral Nucleocapsids. The virus-laden pneumocytes now release many different cytokines and
inflammatory markers such as interleukins (IL-1, IL-6, IL-8, IL-120, and IL-12), tumor necrosis
factor-α (TNF-α), IFN-λ and IFN-β, CXCL-10, monocyte chemoattractant protein-1 (MCP-1) and
macrophage inflammatory protein-1α (MIP-1α). This 'cytokine storm' attracts neutrophils, CD4
helper T cells, and CD8 cytotoxic T cells concealed in lung tissue. These cells battle the virus
but are also responsible for the subsequent inflammation and lung injury. The host cell dies,
releasing more virus particles, infecting the adjacent type 2 alveolar epithelial cells similarly.
Extensive alveolar damage is due to the ongoing injury induced by the sequestered
inflammatory cells and viral replication; this leads to the loss of both type 1 and type 2
pneumocytes, eventually culminating in acute respiratory distress syndrome.

B. Symptoms and Complications

Because the damaged type 2 pneumocytes stop producing surfactant. Without
surfactants, alveolar collapse and gas exchange are not possible. This collection of fluid in the
alveoli, along with alveolar cell damage, alveolar inflammation, and alveolar collapse, can lead
to acute respiratory distress syndrome, where the lungs cannot provide enough oxygen. This is
a life-threatening condition and is the leading cause of death in Covid 19 patients.
COVID-19 has an incubation period of 5-6 days from virus introduction to symptom
manifestation. However, this can be extended to 14 days. During this period, often known as the
'pre-symptomatic' period, infected people can be contagious and spread the virus to healthy
people in the community. COVID-19 patients are primarily between the ages of 40 and 70, and
the most common symptoms are fever, body pains, shortness of breath, malaise, and a dry
cough. However, individuals might have asymptomatic, mild, moderate, or severe disease.
Some patients may experience gastrointestinal symptoms such as stomach pain, vomiting, and
diarrhea. The 'cytokine storm' is primarily responsible for the problems reported in patients with
COVID-19 infection.

C. Diagnosis and Treatment

To confirm the diagnosis, the reverse transcription polymerase chain reaction or RT-
PCR test can be done, which can detect minimal amounts of viral RNA. However, it is worth
mentioning that the RT PCR can often miss the infection early in the disease, which means it is
not very sensitive. So, if severe pulmonary disease is suspected, a chest CT test can be done to
detect viral pneumonia. Next, the pneumorapid testing method for covid 19 can get the result
within minutes. One of these is isothermal Amplification which also checks for viral RNA.
 The other is rapid serological testing which checks for antibodies created by the immune
system to fight the virus. Senses checking for antibodies the body makes can detect previous
infections even after the virus is gone. Finally, looking for other causes of similar symptoms is
also essential. By doing things, for example, like, a quick flu test or respiratory viral panel, to
look for alternative causes of the symptoms.
In terms of treatments, individuals with MILD SYMPTOMS should isolate themselves at
home to improve with rest and fluids. Treatment focuses on supported care for those with
severe symptoms, such as providing ill people with fluids, oxygen, and ventilatory support.

—--------------(HERNEL) END HERE —----------------------------------------------------------------------------

IV. COMPARE AND CONTRAST BETWEEN TB AND COVID

REFERENCES