Calixtro, Laidelle Jascinth M.

BSN-III

NARRATIVE PATHOPHYSIOLOGY OF DIPTHERIA

Diphtheria is an infectious disease caused by the aerobic gram-positive

bacteria Corynebacterium diphtheria, which primarily infects the throat and upper airways, and
produces a toxin affecting other organs. The illness has an acute onset and the main
characteristics are sore throat, low fever and swollen glands in the neck, and the toxin may, in
severe cases, cause myocarditis or peripheral neuropathy. The diphtheria toxin causes a
membrane of dead tissue to build up over the throat and tonsils, making breathing and
swallowing difficult. The disease is spread through direct physical contact or from breathing in
the aerosolized secretions from coughs or sneezes of infected individuals (World Health
Organization, 2018).

The infection usually occurs in the spring or winter months. It is communicable for 2-6
weeks without antibiotic treatment. People who are most susceptible to infection are those who
are not completely immunized or have low antitoxin antibody levels and have been exposed
to a carrier or diseased individual. A carrier is someone whose cultures are positive for the
diphtheria species but does not exhibit signs and symptoms. Pathogenic strains can result in
severe localized upper respiratory infection, localized cutaneous infections, and rarely
systemic infection. Overcrowding, poor health, substandard living conditions, incomplete
immunization, and immunocompromised states facilitate susceptibility to diphtheria and are
risk factors associated with transmission of this disease. Human carriers are the main reservoir
of infection; however, case reports have linked the disease to livestock. Infected patients and
asymptomatic carriers can transmit C diphtheria via respiratory droplets, nasopharyngeal
secretions, and rarely fomites. In the case of cutaneous disease, contact with wound exudates
may result in the transmission of the disease to the skin as well the respiratory tract. Immunity
from exposure or vaccination wanes over time. Inadequate boosting of previously vaccinated
individuals may result in increased risk of acquiring the disease from a carrier, even if
adequately immunized previously.

The prognosis of diphtheria varies from good to poor based on how early the patient is
treated and how the patient reacts to the medication. If the patient has sepsis or bacteremia,
or if there is heart intervention, the prognosis is generally low.

REFERENCES:
Diphtheria. (2020, May 26). Centers for Disease Control and Prevention.
https://www.cdc.gov/diphtheria/index.html

Diphtheria. (2018, September 20). Retrieved February 03, 2021, from

https://www.who.int/immunization/diseases/diphtheria/en/
Calixtro, Laidelle Jascinth BSN-III

NARRATIVE PATHOPHYSIOLOGY OF PERTUSSIS

Pertussis, also known as whooping cough, is a highly contagious respiratory disease.

It is caused by the bacterium Bordetella pertussis. Pertussis is known for uncontrollable,
violent coughing which often makes it hard to breathe. After cough fits, someone with pertussis
often needs to take deep breaths, which result in a “whooping” sound. Pertussis can affect
people of all ages, but can be very serious, even deadly, for babies less than a year old.

This disease's pathophysiology starts as B. Pertussis travels by aerosolized droplets,

binding to and destroying the ciliated respiratory epithelium generated by the cough of infected
individuals. B pertussis also multiplies on the respiratory epithelium, starting in the
nasopharynx and ending primarily in the bronchi and bronchioles. Pertussis is highly
contagious, developing in approximately 80-90% of susceptible individuals who are exposed
to it. Most cases occur in the late summer and early fall. A mucopurulent sanguineous exudate
forms in the respiratory tract. This exudate compromises the small airways (especially those
of infants) and predisposes the affected individual to atelectasis, cough, cyanosis, and
pneumonia. The lung parenchyma and bloodstream are not invaded; therefore, blood culture
results are negative. Transmission of pertussis can occur through direct face-to-face contact,
through sharing of a confined space, or through contact with oral, nasal, or respiratory
secretions from an infected source. Although mothers have historically been the most common
source of transmission of pertussis to their infant, data from a study found that the most
common source of transmission to infants is through their siblings. Young infants, especially
those born prematurely, and patients with underlying cardiac, pulmonary, neuromuscular, or
neurologic disease are at high risk for contracting the disease and for complications.

Prognosis for full recovery from pertussis is excellent in children over 3 months of age.
In those less than 3 months the mortality is 1-3%. Complications of pertussis in older infants
and children are usually minimal, and most patients make a gradual, but full, recovery with
supportive care and antibiotics. Minor complications during the illness include epistaxis,
nausea and vomiting, subconjunctival hemorrhages, and ulcers of the frenulum.

REFERENCES:

Bocka, J., MD. (2019, November 13). Pertussis. Retrieved February 03, 2021, from
https://emedicine.medscape.com/article/967268-overview#a6

Cheever, K. H., & Hinkle, J. L. (2018). Brunner & Suddarth's textbook of medical-surgical
nursing. Philadelphia: Wolters Kluwer.

Pertussis. (2019, November 18). Retrieved February 03, 2021, from

https://www.cdc.gov/pertussis/index.html#:~:text=Pertussis%2C%20also%20known%2
0as%20whooping,makes%20it%20hard%20to%20breathe.
Calixtro, Laidelle Jascinth M. BSN-III

NARRATIVE PATHOPHYSIOLOGY OF TUBERCULOSIS

Tuberculosis (TB) is caused by a bacterium called Mycobacterium tuberculosis. The bacteria usually
attack the lungs, but TB bacteria can attack any part of the body such as the kidney, spine, and brain. Some
people develop TB disease soon after becoming infected (within weeks) before their immune system can
fight the TB bacteria. Other people may get sick years later, when their immune system becomes weak for
another reason. The risk factors for acquiring TB include close-contact situations, alcohol and IV drug abuse,
and certain diseases (for example, diabetes, cancer, and HIV) and occupations (for example, health-care
workers).

The pathophysiology begins when an individual inhales a Mycobacterium which travels down the
airways into the alveoli. Here the Mycobacterium will start to multiply, and in some cases, bacilli may also
travel across the body through the lymphatic system. The infection may occur anywhere between 2 to 20
weeks after being exposed to the Mycobacterium. Naturally, the body goes in Defense Mode and starts an
inflammatory reaction. This allows the bacteria to be engulfed by Phagocytes, and the bacilli to be destroyed
by TB Specific Lymphocytes. However, while the TB Specific Lymphocytes are busy attacking the bacilli,
they are also attacking healthy tissue. The breakdown of normal tissue will lead to a build-up of Exudate in
the alveoli, which in turn causes Bronchopneumonia. The live and dead bacilli start to accumulate and form
Granulomas, which over time transform into a Fibrous Mass. The center part of this fibrous mass is called
Ghon Tubercle. Eventually, some of the bacteria and macrophages from the Fibrous Mass become necrotic
and form a slimy mass. Which in turn will calcify and create collagenous scars. At this point, the bacteria will
sleep, and there is no more advancement of active disease. After the first infection is over, the active disease
might come back if the person does not have a strong immune system, or if he gets re-infected. In the case
of re-infection, the Ghon Tubercle ulcerates and pushes the bacteria out into the bronchi. Here, the bacteria
will become airborne and increase the chances of infecting other people. The ulcers on the Ghon Tubercle
will eventually close up and form even more scar tissue. Naturally, the build-up of scar tissue will irritate the
lung, so the lung becomes more inflamed, which creates more Tubercle and develops Bronchopneumonia.

TB is a severe and often deadly disease without treatment. Long-term prognosis for treated patients
with TB is good. The right treatment can cure about 90 percent of the patients. People who have Tb have to
be on medication for about 6 to 9 months. Most people get better in a few weeks, but the bacteria is still in
the body.

REFERENCES:

TB Risk Factors | Basic TB Facts | TB | CDC. (2021). Retrieved 18 February 2021, from
https://www.cdc.gov/tb/topic/basics/risk.htm

Topics, H. (2021). Tuberculosis | TB | TB Test | MedlinePlus. Retrieved 18 February 2021, from

https://medlineplus.gov/tuberculosis.html
Calixtro, Laidelle Jascinth M. BSN-III

NARRATIVE PATHOPHYSIOLOGY OF PNEUMONIA

Pneumonia can be identified as a lung parenchymal infection in which the

consolidation of the infected part and the filling of the alveolar air with exudate, inflammatory
cells and fibrin are characteristic. Bacterial pneumonia is caused by a pathogenic infection of
the lungs and may present as a primary disease process or as the final coup de grace in the
individual who is already debilitated. For example, a historical review of the 1918-19
influenza pandemic suggests that the majority of deaths were not a direct effect of the
influenza virus, but they were from bacterial co-infection. Pneumonia can range in
seriousness from mild to life-threatening. It is most serious for infants and young children,
people older than age 65, and people with health problems or weakened immune systems.
The pathophysiology begins when the bacteria from the upper airways or, less
commonly, from hematogenous spread, find their way to the lung parenchyma. Once there,
a combination of factors (including virulence of the infecting organism, status of the local
defenses, and overall health of the patient) may lead to bacterial pneumonia. The patient
may be made more susceptible to infection because of an overall impairment of the immune
response (eg, human immunodeficiency virus [HIV] infection, chronic disease, advanced
age) and/or dysfunction of defense mechanisms (eg, smoking, chronic obstructive
pulmonary disease [COPD], tumors, inhaled toxins, aspiration). Poor dentition or chronic
periodontitis is another predisposing factor. Thus, during pulmonary infection, acute
inflammation results in the migration of neutrophils out of capillaries and into the air spaces,
forming a marginated pool of neutrophils that is ready to respond when needed. These
neutrophils phagocytize microbes and kill them with reactive oxygen species, antimicrobial
proteins, and degradative enzymes. They also extrude a chromatin meshwork containing
antimicrobial proteins that trap and kill extracellular bacteria, known as neutrophil
extracellular traps (NETs). Various membrane receptors and ligands are involved in the
complex interaction between microbes, cells of the lung parenchyma, and immune defense
cells. Bacterial pneumonia's clinical presentation varies. Bacterial pneumonia is synonymous
with the abrupt onset of symptoms and the quick progression of the disease. The pulmonary
mechanism is also highly indicative of chest pain, dyspnea, hemoptysis (when specifically
delineated from hematemesis), decreased exercise tolerance, and abdominal pleuritis pain.
The presence of cough is the most persistent clinical manifestation, particularly cough
productive of sputum.

Generally, the prognosis is good in otherwise healthy patients with uncomplicated

pneumonia. Advanced age, aggressive organisms (eg, Klebsiella, Legionella, resistant S
pneumoniae), comorbidity, respiratory failure, neutropenia, and features of sepsis, alone or
in combination, increase morbidity and mortality. Left untreated, pneumonia may have an
overall mortality rate of more than 30%.

REFERENCES:

Justina Gamache, M. (2020, December 06). Bacterial pneumonia clinical presentation:

History, physical examination, risk stratification. Retrieved February 20, 2021, from
https://emedicine.medscape.com/article/300157-clinical

Pneumonia - Symptoms and causes. (2020). Mayo Clinic;

https://www.mayoclinic.org/diseases-conditions/pneumonia/symptoms-causes/syc-
20354204#:~:text=Pneumonia%20is%20an%20infection%20that,and%20fungi%2C%
20can%20cause%20pneumonia
Calixtro, Laidelle Jascinth M. BSN-III

NARRATIVE PATHOPHYSIOLOGY OF MENINGOCOCCEMIA

Meningococcemia is a rare infectious disease characterized by upper respiratory tract

infection, fever, skin rash and lesions, eye and ear problems, and possibly a sudden state of
extreme physical depression (shock) which may be life-threatening without appropriate medical
care. It is caused by the bacteria Neisseria meningitides which is the same type of bacteria that
can cause meningitis. When the infection remains in the blood but does not infect the brain or
spinal cord, it is called meningococcemia. There are two forms of meningococcemia. Fluminant
meningococcemia develops very rapidly and is more severe than chronic meningococcemia,
which has a waxing and waning course.Babies, children, and young adults have a higher risk of
acquiring this disease.

Generalized vascular damage, marked by endothelial necrosis, intraluminal thrombosis,

and perivascular hemorrhage, is the major pathological alteration in meningococcemia. The
vascular endothelium is damaged by endotoxins, cytokines, and free radicals, causing platelet
deposition and vasculitis. By inducing extreme hypotension, decreased cardiac output and
increased endothelial permeability, the deleterious effects of cytokines play a significant role in
the pathogenesis of meningococcemia. The clinical picture of meningococemia is the product of
intravascular compartmental infection and intracranial bacterial growth and inflammation. The
pathogen binds to the endothelial cells by type IV pili. This results in microcolonies on the apical
portion of the endothelial cell. Multiple organ failure, shock, and death may ensue as a result of
anoxia in vital organs and massive disseminated intravascular coagulation. Patients with
fulminant meningococcemia develop thrombosis and hemorrhage in the skin, the mucous
membranes, the serosal surfaces, the adrenal sinusoids, and the renal glomeruli. Adrenal
hemorrhage is rarely extensive. Thrombosis of the glomerular capillaries may cause renal
cortical necrosis, the chief characteristic of the generalized Shwartzman reaction, which is a
model of DIC. Thrombi containing numerous leukocytes are occasionally found in the lungs, and
extensive intra-alveolar hemorrhage can occur. Myocarditis, when it occurs, carries a poor
prognosis with a high mortality risk.

Meningococcal disease can progress very quickly and can result in loss of life,
neurologic impairment, or peripheral gangrene. Patients with terminal complement component
deficiency have a more favorable prognosis. A fatal outcome is highly associated with properdin
deficiencies. Coagulopathy with a partial thromboplastin time of greater than 50 seconds or a
fibrinogen concentration of less than 150 µg/dL are also markers of poor prognosis.

REFERENCES:

Mahmud H Javid, MBBS. (2020, December 6). Meningococcemia: Practice Essentials,

Background, Pathophysiology. Medscape.com; Medscape.
https://emedicine.medscape.com/article/221473-overview#a6
Meningococcemia. (n.d.). Retrieved February 20, 2021, from https://rarediseases.org/rare-
diseases/meningococcemia/

Holm, G. (2018, June 5). Meningococcemia: Causes, Symptoms, and More. Healthline;
Healthline Media. https://www.healthline.com/health/meningococcemia
Calixtro, Laidelle Jascinth M. BSN-III

NARRATIVE PATHOPHYSIOLOGY OF MENINGITIS

Meningitis is an inflammation (swelling) of the protective membranes covering the

brain and spinal cord. A bacterial or viral infection of the fluid surrounding the brain and
spinal cord usually causes the swelling. However, injuries, cancer, certain drugs, and other
types of infections also can cause meningitis. Bacterial meningitis is a bacterial infection of
the meninges, which is the protective covering for the brain and spinal cord resulting in
inflammation. It is a serious and life-threatening condition that requires prompt diagnosis and
treatment

Bacterial meningitis Bacterial meningitis is generally a serious infection. It is caused

by three types of bacteria: Haemophilus influenzae type B, Neisseria meningitidis, and
Streptococcus pneumoniae bacteria. Meningitis caused by Neisseria meningitides is known
as meningococcal meningitis, while meningitis caused by Streptococcus pneumoniae is
known as pneumococcal meningitis. People become infected when they are in close contact
with the discharges from the nose or throat of a person who is infected. The bacteria then
cross the mucus layer and enter the bloodstream. If the body’s immune response cannot
clear the bacteria at this point, then they may start to multiply uncontrollably in the
bloodstream causing severe damage to the lining of the blood vessels and resulting in
septicemia. Bacteria may also invade the cerebrospinal fluid and the meninges, which leads
to inflammation in this area, resulting in meningitis. A combination of the body’s own immune
response and toxins produced by the bacteria cause the damage to the meninges.

The prognosis in patients with meningitis caused by opportunistic pathogens

depends on the underlying immune function of the host. Many patients who survive the
disease require lifelong suppressive therapy (eg, long-term fluconazole for suppression in
patients with HIV-associated cryptococcal meningitis). Untreated bacterial meningitis is
almost always fatal. With treatment the risk of death is reduced. In new-borns the risk of
death with treatment is 20 to 30%, in older children it is around 2% with treatment. The death
risk is higher for adults even with treatment at 19 to 37%.

REFERENCES:

Meningitis. (2020, January 21). Retrieved February 01, 2021, from

https://www.cdc.gov/meningitis/index.html#:~:text=Meningitis%20is%20an%20inflamm
ation%20(swelling,infections%20also%20can%20cause%20meningitis.

Rodrigo Hasbun, M. (2019, November 11). Meningitis. Retrieved February 01, 2021, from
https://emedicine.medscape.com/article/232915-overview#a6

Runde TJ, Anjum F, Hafner JW. Bacterial Meningitis. [Updated 2020 Dec 4]. In: StatPearls
[Internet]. Treasure Island (FL): StatPearls Publishing; 2020 Jan-. Available from:
https://www.ncbi.nlm.nih.gov/books/NBK470351/
Calixtro, Laidelle Jascinth M. BSN-III

BACILLARY DYSENTERY OR SHIGELLA NARRATIVE PATHOPHYSIOLOGY

Dysentery refers to diarrhea with blood and/or mucus. Bacillary dysentery is a

bacterial dysentery caused by Shigella infection. Shigella spp. can cause intestinal
inflammation and symptoms of gastroenteritis without dysentery. Shigella is a genus of
aerobic, non-motile, glucose-fermenting, Gram-negative bacilli that are highly contagious.
Man and apes appear to be the only natural hosts. They cause damage by invasion of the
colonic epithelium causing intense inflammation, and by the injection of type III effector
proteins into host cells thereby altering their function. It is widespread and results from
contaminated food, poor sanitation conditions, or direct interaction with people. In all age
groups, Shigella can cause infection. Very young, elderly, and immunocompromised people
are included in the high risk category. The species of Shigella is surprisingly immune to
stomach acids, and few organisms are required to cause the disease.

When the bacteria are ingested, the pathophysiology of the disease begins It
multiplies in the small intestine once ingested and enters the colon. Shigella enterotoxins
and serotype toxin 1 are produced in the colon, resulting in watery or bloody diarrhea.
Morover, when there is a multiplication in the mucosa and results in the production of
endotoxin that affects the lining of the small intestines, colon, and capillary, leading to
mucosal layer necrosis. Ulceration that leads to gangrene and toxemia could occur. Clinical
manifestations generally result in the ingestion of the organism within 12 hours to 3 days,
with an average incubation period of 3 days. These symptoms include high fever, vomiting,
diffuse colicky abdominal pain followed by bloody mucoid diarrhea and tenesmus. It self-
resolves within 5 to 7 days of onset of symptoms. However, high-risk individuals may end up
with complications.

The disease tends to last from one day to one month with an average of one week.
The more common form in the UK usually lasts for up to a week, whereas the tropical forms
tend to be more severe and last for 2-4 weeks. Mortality is rare but can occur in
malnourished children and the elderly.

REFERENCE:
Aslam A, Okafor CN. Shigella. [Updated 2020 Aug 11]. In: StatPearls [Internet].
Treasure Island (FL): StatPearls Publishing; 2020 Jan-. Available from:
https://www.ncbi.nlm.nih.gov/books/NBK482337/

Harding, D. (2016, May 25). Bacillary dysentery. what is bacillary Dysentery? Information.
Retrieved February 19, 2021, from https://patient.info/doctor/shigellosis

Joyann A Kroser, M. (2019, November 10). Shigellosis. Retrieved February 19, 2021, from
https://emedicine.medscape.com/article/182767-overview
Calixtro, Laidelle Jascinth M. BSN-III

NARRATIVE PATHOPHYSIOLOGY OF BOTULISM

Botulism is a rare but serious illness caused by a toxin that attacks the body’s nerves
that transmits through food, contact with contaminated soil, or through an open wound.
Botulism poisoning is due to a toxin formed by Clostridium botulinum, a form of bacteria. These
bacteria, while very widespread, can only survive in environments where there is no oxygen.
A potent breeding ground is created by some food sources, such as home-canned foods.

Toxin-mediated blockage of neuromuscular signaling of cholinergic nerve fibers is

implicated in the pathophysiology of this disease. This is done either by inhibiting the release
of acetylcholine at the myoneural junctions' presynaptic clefts or by binding acetylcholine itself.
Toxins are absorbed from the stomach and small intestine, where they are not denatured by
digestive enzymes. Consequently, they are hematogenously disseminated and block
neuromuscular transmission in cholinergic nerve fibers. The nervous, gastrointestinal,
endocrine, and metabolic systems are predominantly affected. Because the motor end plate
responds to acetylcholine, botulinum toxin ingestion results in hypotonia that manifests as
descending symmetric flaccid paralysis and is usually associated with gastrointestinal
symptoms of nausea, vomiting, and diarrhea. Cranial nerves are affected early in the disease
course. Later complications include paralytic ileus, severe constipation, and urinary retention.
Wound botulism results when wounds are contaminated with C botulinum spores. Wound
botulism has developed following traumatic injury that involved soil contamination, among
injection drug users (particularly those who use black-tar heroin), and after cesarean delivery.
The wound may appear deceptively benign. Traumatized and devitalized tissue provides an
anaerobic medium for the spores to germinate into vegetative organisms and to produce
neurotoxin, which then disseminates hematogenously. The nervous, endocrine, and metabolic
systems are predominantly affected. Symptoms develop after an incubation period of 4-14
days, with a mean of 10 days. The clinical symptoms of wound botulism are similar to those
of foodborne botulism except that gastrointestinal symptoms (including nausea, vomiting,
diarrhea) are uncommon. Symptoms of botulism usually start with weakness of the muscles
that control the eyes, face, mouth, and throat. This weakness may spread to the neck, arms,
torso, and legs. Botulism also can weaken the muscles involved in breathing, which can lead
to difficulty breathing and even death.

The prognosis for Botulism is good. Although botulism can cause severe and
prolonged symptoms, most people recover completely from the illness. Early treatment
reduces the risk of permanent disability and death. However, even with treatment botulism
can be fatal. Without treatment, more than 50% of people with botulism would die.

REFERENCES:

Chan, K., MD. (2019, November 11). Botulism. Retrieved February 01, 2021, from
https://emedicine.medscape.com/article/213311-overview#a6

Cheever, K. H., & Hinkle, J. L. (2018). Brunner & Suddarth's textbook of medical-surgical
nursing. Philadelphia: Wolters Kluwer.
Raynolds, J., MD. (2018, August 13). Botulism. Retrieved February 01, 2021, from
https://www.health.harvard.edu/a_to_z/botulism-a-to-z

Symptoms. (2018, October 04). Retrieved February 02, 2021, from

https://www.cdc.gov/botulism/symptoms.html
Calixtro, Laidelle Jascinth M. BSN-III

NARRATIVE PATHOPHUSIOLOGY OF TYPHOID FEVER

Typhoid fever or also known as enteric fever is a life-threatening infection caused by

the bacterium Salmonella Typhi. Typhoid fever and paratyphoid fever are life-threatening
illnesses caused by Salmonella serotype Typhi and Salmonella serotype Paratyphi,
respectively. Typhoid fever, the most severe type of salmonellosis, typically lasts between 1 -
4 weeks. It is triggered by contact with the gram-negative bacteria salmonella typhi or
salmonella paratyphi, which is generally foodborne. The disease can also spread through
contact with infected persons or animals and through fecal-oral spread in small children.
Typhoid fever typically occurs from drinking water infected by carrier excretion.

S. typhi and paratyphi enter the host's system primarily through the distal ileum. They
have specialized fimbriae that adhere to the epithelium over clusters of lymphoid tissue in the
ileum (Peyer patches), the main relay point for macrophages traveling from the gut into the
lymphatic system. After contaminated food is ingested, the bacteria pass the gastric barrier
and invade the upper small bowel, causing a transient bacteremia that produces no symptoms.
The bacteria then induce their host macrophages to attract more macrophages. The bacteria
are ingested by mononuclear phagocytes and must survive and multiply within them to cause
illness. The bacteria then infect the gallbladder via either bacteremia or direct extension of
infected bile. The result is that the organism re-enters the gastrointestinal tract in the bile and
reinfects Peyer patches. Bacteria that do not reinfect the host are typically shed in the stool
and are then available to infect other hosts.

Generally, untreated typhoid fever has a mortality rate of 15-30 per cent. In a well
treated illness, the death rate is less than 1%. Unspecific percentages of people suffer long-
term or lasting risks, including neuropsychiatric problems and elevated incidence of
gastrointestinal cancer.

REFERENCES:

Typhoid fever treatment & management: Medical care, surgical care, consultations. (2019,
November 11). Diseases & Conditions - Medscape Reference.
https://emedicine.medscape.com/article/231135-treatment

Typhoid fever. (n.d.). Retrieved February 03, 2021, from https://www.who.int/news-room/q-

a-detail/typhoid-
fever#:~:text=Typhoid%20fever%20is%20a%20life,patients%20may%20have%20a%2
0rash.

 Calixtro, Laidelle Jascinth M. BSN-
NARRATIVE PATHOPHYSIOLOGY OF LEPROSY

Leprosy (also known as Hansen’s Disease) is an infection caused by slow-growing

bacteria called Mycobacterium leprae. It can affect the nerves, skin, eyes, and lining of the nose
(nasal mucosa). With early diagnosis and treatment, the disease can be cured. People with
Hansen’s disease can continue to work and lead an active life during and after treatment.
Leprosy is known to occur at all ages ranging from early infancy to very old age. Transmission
of leprosy is accepted to be primarily person-to-person via repeated contact with nose
and mouth droplets from someone with untreated leprosy. The risk of developing leprosy is 5–
10 times higher if one member of the family has developed the disease previously. (Centers For
Disease Control and Prevention, 2020). Leprosy can be classified into three types namely
Tuberculoid, Lepromatous, and Borderline. A person’s immune response to the disease
determines which of these types of leprosy they have. In tuberculoid leprosy, the immune
response is good. A person with this type of infection only exhibits a few lesions. The disease is
mild and only mildly contagious. While In lepromatous leprosy, the immune response is
poor. This type also affects the skin, nerves, and other organs. There are widespread lesions,
including nodules (large lumps and bumps). This form of disease is more contagious.Lastly, In
borderline leprosy, there are clinical features of both tuberculoid and lepromatous leprosy. This
type is considered to be between the other two types.

As a person with leprosy coughs or sneezes, droplets containing the M. leprae bacteria
may spread and another person may inhale it. When these are released into the environment,
they can be inhaled by other susceptible persons. The bacilli enter through respiratory tract, it
infects what are called Schwann cells and replicate inside the Schwann cells. It primarily
affects Schwann cells in the peripheral nerves, especially the ulnar, radial, posterior-popliteal,
anterior-tibial and facial nerves leading to nerve damage, demyelination and the development
of the disabilities. The areas that are commonly affected by leprosy tend to be the cooler parts
of the body. If they attack a large nerve trunk, motor nerve damage, weakness and pain occur,
followed by peripheral anesthesia, muscle paralysis and atrophy.

Prognosis of leprosy varies on various factors such as stage of disease at diagnosis,

early initiation of treatment, patient's access to treatment, and compliance with therapy.
Without treatment, leprosy can lead to permanent muscle weakness, nerve damage, and
disfiguration. Even with treatment, recovery from neurologic impairment is limited, but skin
lesions generally clear within the first year of therapy. Discoloration and skin damage typically
persist.

REFERENCES:

Leprosy - StatPearls - NCBI bookshelf. (2020, November 23). National Center for Biotechnology
Information. https://www.ncbi.nlm.nih.gov/books/NBK559307/
Leprosy: Background, pathophysiology, epidemiology. (2020, June 30). Diseases & Conditions
Medscape Reference. https://emedicine.medscape.com/article/220455-overview#a5
Transmission. (2017, February 10). Retrieved February 06, 2021, from
https://www.cdc.gov/leprosy/transmission/index.html
Calixtro, Laidelle Jascinth M. BSN-III

NARRATIVE PATHOPHYSIOLOGY OF ANTHRAX

Anthrax is a rare but serious illness caused by a spore-forming bacterium, gram-positive,

rod-shaped, Bacillus anthracis. It primarily affects livestock and wild animals. People can get
sick with anthrax if they come in contact with infected animals or contaminated animal products.
Anthrax can cause severe illness in both humans and animals.

Its pathophysiology starts when the bacteria that infect the individual release the toxin,
culminating in hemorrhage, edema, and necrosis. The incubation period is between 1 and 6
days. There are three primary types of infection: contact with the skin, inhalation and
gastrointestinal absorption. Skin lesions trigger pruritus edema and macule or papule formation,
resulting in ulceration of 1-to 3-mm vesicles. A painless eschar develops, which falls within 1 to
2 weeks. Fever, nausea and vomiting, abdominal pain, bloody diarrhea, and occasionally
ascites will manifest when an anthrax is ingest. As severe diarrhea develops, decreased
intravascular volume becomes the primary concern for treatment. The bacterium targets at the
terminal of ileum and cecum. Sepsis may occur. Inhalation of anthrax results in the most serious
clinical manifestations. Its symptoms are similar to those of the flu, and treatment usually took
only when the second stage of severe respiratory distress occurs. Current antibiotic therapy
does not stop the progress of the disease. Inhaled anthrax may incubate for up to 60 days,
making it difficult to identify its source. Initial signs and symptoms include cough, headache,
fever, vomiting, chills, weakness, mild chest discomfort, dyspnea, and syncope, with no
rhinorrhea or nasal congestion. Most patients have a short recovery period followed by a
second stage within 1 to 3 days, characterized by fever, severe respiratory distress, stridor,
hypoxia, cyanosis, diaphoresis, hypotension, and shock. These patients require optimisation of
oxygenation, correction of electrolyte imbalances and ventilatory and hemodynamic support. A
hemorrhagic mediastinitis may also be apparent on the chest x-ray (a hallmark sign). The
disease may also develop into meningitis with subarachnoid hemorrhage causing complications.

As long as there is an early detection and prompt management of antibiotics, the

prognosis of Anthrax is good. The anthrax mortality rate varies, depending on exposure, and is
approximately 20 percent for skin anthrax without antibiotics and 25-75 percent for
gastrointestinal anthrax; the anthrax inhalation rate is 80 percent or higher.

REFERENCES:

Anthrax. (2020, May 15). Retrieved February 20, 2021, from

https://www.mayoclinic.org/diseases-conditions/anthrax/symptoms-causes/syc-20356203

Center for Biologics Evaluation and Research. (2020). Anthrax. U.S. Food and Drug
Administration. https://www.fda.gov/vaccines-blood-biologics/vaccines/anthrax
Cheever, K. H., & Hinkle, J. L. (2018). Brunner & Suddarth's textbook of medical-surgical
nursing. Philadelphia: Wolters Kluwer.

What is anthrax? (2020, November 20). Retrieved February 20, 2021, from
https://www.cdc.gov/anthrax/basics/index.html#:~:text=Anthrax%20is%20a%20serious%2
0infectious,wild%20animals%20around%20the%20world.