CASE STUDY IN MICRO – PARA

I. NAME OF DISEASE
II. ETIOLOGY ( SIGNS AND SYMPTOMS)
III. DIAGNOSTIC PROCEDURE
IV. MEDICAL MANAGEMENT
V. NURSING INTERVENTION
VI. PATOPHYSIOLOGY

Submitted to :
Mr. Rommel S. Aninag

Submitted by :
Cherry Ann A. Masiglat
ENDEMIC DISEASES
I. NAME OF THE DISEASE

- CHICKEN POX

II. ETIOLOGY

Chickenpox is caused by the varicella-zoster virus, which also

causes shingles. Chickenpox is highly contagious and spreads by
closeness and contact with someone with chickenpox. Fever, malaise,
and a very itchy rash (red spots, fluid-filled tiny blisters, and crusted
lesions) are all signs and symptoms of chickenpox. Chickenpox is
caused by varicella-zoster virus transmitted through respiratory
droplets. Direct contact with papules and vesicles (not crusts) can also
spread the virus. Neonatal varicella is when the is when the mother
develops chickenpox during pregnancy and it is spread across the
placenta to the fetus. The patient is contagious within 48 hours after
exposure and may continue to spread the virus until spots crust over.
Anyone who has not had chickenpox or shingles which comes from the
same virus. After having chickenpox once, the body creates antibodies
to the disease and the virus becomes dormant in the nerve tissue.

III. DIAGNOSTIC PROCEDURE

The most sensitive method for confirming a diagnosis of varicella

is the use of polymerase chain reaction (PCR) too detect VZV in skin
lesions (vesicles, scabs, maculopapular lesions). Vesicular lesions or
scabs, if present are the best for sampling.

IV. MEDICAL MANAGEMENT

If you or your child are at high risk of complications, your doctor

may suggest an antiviral drug such as acyclovir (Zovirax, Sitavig) or
another drug called immune globulin intravenous (Privigen). These
medications may lessen the severity of chickenpox when given within
24 hours after the rash first appears.

V. NURSING INTERVENTIONS

 Perform physical assessment.

Get baseline to determine effectiveness of interventions. Note
stage of disease : active, fluid filled blisters or scabbed and
crusted lesions.
 Monitor vital signs
 Fever often companies a chickenpox outbreak. Other changes in
vital signs can indicate development of systemic infection.
 Assess skin for signs of secondary infection.
Itching leads to open wounds which are a breeding ground for
bacteria and infection.
 Trim nails or cover hands of infants and toddlers.
Keeping the nails short or covered helps prevent scratches inn the
skin that can lead to infection.
 Encourage rest.
When the body is resting, more energy can be devoted to
healing. This can also help to minimize fatigue and discomfort.
 Manage with cool compresses or tepid baths with oatmeal or
cornstarch.
To help relieve itching and soothe irritated skin.
 Administer medications appropriately
o Oral antivirals
o Oral antihistamine
o Oral or recta
o Acetaminophen
o Topical calamine
1. Avoid giving aspirin or other salicylates to children with viral
illnesses due to risk for Reye’s Syndrome.
 Antiviral (acyclovir) medications may help lessen the severity or
shorten the duration of the disease.
 Antihistamines (diphenhydramine) are given to relieve itching.
 Acetaminophen is often given to treat fever and pain.
 Calamine lotion cream or gel may be applied to help relieve
itching and discomfort.
  Encourage hydration
Water is better than sugary drinks to maintain hydration, even if
child has a little appetite. Children may be more responsive to
popsicles for replacement of fluid and electrolytes.
 Provide education for patient and parents regarding :
o Preventing the spread of the disease
o Infection control
o Vaccines
o When to return to school/daycare
 The virus can be spread to others until all lesions have crusted
over, therefor, the child should not return to school or daycare
until they are no longer contagious, even if feeling better.
 Good hand hygiene can help spread infection.
 Varicella vaccine may be given 3 – 5 days after exposure (before
symptoms begin) to prevent or lessen the severity of the disease.
All children over 12 months of age should be vaccinated.

VI. PATHOPYSIOLOGY

Varicella, more commonly known chickenpox, is a viral infection

that causes an itchy rash with small blisters on the skin and flu-like
symptoms. Chickenpox is highly contagious and usually affects children.
A red, intensely itchy rash in the hallmark sigh of chickenpox and may
develop anywhere on the body including the scalp, mouth, arms, legs,
trunk and genitals. Symptoms normally begin within 10 – 21 days after
exposure to the virus and last 1 – 2 weeks. The varicella vaccine is
routinely given to children at the ages of 12 months and 4 years old
and is highly effective in preventing the disease.
I. NAME OF THE DISEASE

- MALARIA

Malaria is caused by the Plasmodium parasite. The parasite can

be spread to humans through the bites of infected mosquitoes. There
are many different types of plasmodium parasite, but only 5 types
cause malaria in humans.
These are :

 Plasmodium falciparum – mainly found in Africa, it’s most

common type of malaria parasite and is responsible for most
malaria deaths worldwide.
 Plasmodium vivax – Mainly found in Asia and South America,
this parasite causes milder symptoms than Plasmodium
falciparum, but it can stay in the liver for up to 3 years, which can
result in relapses.
 Plasmodium ovale – fairly uncommon and usually found in West
Africa, it can remain in your liver for several years without
producing symptoms.
 Plasmodium malariae – this is quite rare and usually found in
Africa.
 Plasmodium knowlesi – this is very rare and found in parts of
Southeast Asia.

II. ETIOLOGY

The symptoms of malaria typically develop within 10 days to 4

weeks following the infection. In some cases, symptoms may not
develop for several months. Some malarial parasites can enter the
body but will be dormant for long periods of time.

Common symptoms of malaria includes :

 Shaking chills that can range from moderate to severe

 High fever
 Profuse sweating
 Headache
  Nausea
 Vomiting
 Abdominal pain
 Diarrhea
 Anemia
 Muscle pain
 Convulsions
 Coma
 Bloody stools


III. DIAGNOSTIC PROCEDURES

Your doctor will be able to diagnose malaria. During your

appointment, your doctor will review your health history, including any
recent travel to tropical climates. A physical exam will also be
performed.

Your doctor will be able to determine if you have an enlarged

spleen or liver. If you have symptoms of malaria, your doctor may
order additional blood tests to confirm your diagnosis.

The tests will show :

 Whether you have malaria

 What type of malaria you have
 If your infection is caused by a that’s resistant to certain types of
drugs
 If the disease has caused anemia
 If the disease has affected your vital organs.
IV. MEDICAL MANAGEMENT

 Artemisinin-based combination therapies (ACTs). ACTs are, in

many cases, the first line treatment for malaria. There are several
different types of ACTs. Examples include artemether-
lumefantrine (Coartem) and antesunate-amodiaquine. Each ACT is
a combination of two or more drugs that work against the malaria
parasite in different ways.
 Chloroquine phosphate. Chloroquine is the preferred treatment
for any parasite that is sensitive to the drug. But in many parts of
the world, the parasites that cause malaria are resistant to
chloroquine, and the drug is no longer an effective treatment.
 Combination of atovaquone and proguanil (Malaronen)
 Quinine sulphate (Qualaquin) with doxycycline ( Vibramycin,
Monodox, others)
 Mefloquine
 Primaquine


V. NURSING INTERVENTION

 Improve body temperature. Warm water compress on forehead

and both axilla (not more than 15 minutes each time) ; maintain
warm environment by using warm blankets, adequate clothing) ;
patient may sweat excessively, make sure to avoid exposing
patient to wet clothes and linens ; administration of antipyretic
drug as ordered.
 Improve tissue perfusion. Patient may need supplemental oxygen
if condition is severe; maintain a well-ventilated room; head to
 bed at 30° ; lessen activities that require moderate to high
exertion.
 Improve fluid volume. Expect loss of fluid through sweat ; provide
information about fluid balance and guideline for fluid
replacement ; encourage increase in oral fluid replacement ;
encourage increase in oral fluid intake ; administer parenteral
fluids as ordered.
 Educate the patient and family. Review the disease process and
therapy, focusing on patient’s concerns ; discuss importance of
adhering to therapy ; go over medication, purpose, frequency,
dosage and side effects ; have a family member or trusted
individual listen to and understand guideline of treatment as the
patient chooses.

VI. PATHOPYSIOLOGY

The natural history of malaria involves cyclical infection of

humans and female Anopheles Mosquitoes.

 In humans, the parasites grow and multiply first in the liver cells
and then in the red cells of the blood.
 In the blood, successive broods of parasites grow inside the red
cells and destroy them, releasing daughter parasites
(“merozoites”) that continue the cycle by invading other red cells.
 The blood-stage parasites are those that cause the symptoms of
malaria ; when certain forms of blood stage parasites
(gametocytes, which occur in male and female forms) are
ingested during blood feeding by a female Anopheles Mosquito,
 they mate in the gut of the mosquito and begin a cycle of growth
and multiplication in the mosquito.
 After 10 – 18 days, a form of the parasite called sporozite
migrates to the mosquito’s salivary glands.
 When the Anopheles mosquito takes a blood meal on another
human, anticoagulant saliva is injected together with the
sporozites, which migrate to the liver, thereby beginning a new
cycle.
 Thus infected mosquito carries the disease from one human to
another (acting as a “vector”, while infected humans transmit the
parasite to the mosquito.
 In contrast to the human host, the mosquito vector does not
suffer from the presence of the parasites.
EPIDEMIC DISEASES
I. NAME OF THE DISEASE

- MENINGOCOCCEMIA

Meningococcemia is a rare infection caused by the Neisseria

meningitides bacteria. This is the same type of bacteria that can cause
meningitis. When the bacteria infect the membranes that cover the
brain and spinal cord, it’s called meningitis.
II. ETIOLOGY

Meningococcemia is characterized by sudden intense headache,

nausea, fever, vomiting and skin rash. The affected individual may first
complain of an upper respiratory infection. Chills may develop, the skin
rash on the arms or legs and the trunk. Diarrhea may also be present.

III. DIAGNOSTIC PROCEDURE

Meningococcemia – is usually diagnosed through blood tests. Your

doctor will take a sample of your blood and then do a blood culture to
determine if bacteria are present. Your doctor may perform a culture
using fluid from your spine instead of your blood.

IV. MEDICAL MANAGEMENT

Because mortality may be reduced with early antibiotic therapy,

patients with a meningococcal rash should receive parental antibiotics
by means on an intravenous (IV) or intramuscular (IM) route as soon as
the diagnosis is suspected.

 Chomoprophylaxis. Chromoprophylaxis for meningococcal

infection should be administered to intimate household, daycare
center, and nursery school contacts. Ciprofloxacin, ceftriaxone,
and rifampicin are the most common antibiotic given as
chemoprophylaxis.
 Diet. Patients with meningitis or fulminant meningococcemia are
at risk of vomiting and should be prevented from taking anything
by mouth prior to substantial clinical improvement with
antimicrobial therapy.
 Activity. The level of patient activity is determined by the severity
of the presentation ; bed rest is recommended for patients
suspected of having meningococcal disease ; in most severe cases,
patients are bed bound.
 Vaccination. The conjugate vaccine for group C meningococci in
which the serogroup C meningococcal polysaccharide is
conjugated to the protein CRM197 appears to provide
immunogenic protection to young children> It was administered
to all children during 1999 – 2000.

V. NURSING INTERVENTION

 Increase cerebral perfusion. Monitor vital signs and

neurological status ; observe for any signs of increased
intracranial pressure ; observe for increasing restlessness,
moaning and guarding behaviours ; maintain head or neck in
midline position, provide bending of the knee and pushing
heels against the mattress ; elevate the head of the bed 30° ,
and avoid neck flexion and hip flexion.
 Improve body temperature. Assess for signs of dehydration
such as dry mouth, sunken eyes, sunken fontanelle, low
concentrated urine output ; gradually decrease temperature by
performing tepid sponge bath ; maintain adequate fluid intake
as tolerated ; and administer antipyretics as indicated.
  Decrease pain. Maintain a quiet environment and keep child’s
room darkened ; turn the client often and position the client
carefully ; prevent stimulation and restrict visitors ; control
environment to encourage rest ; and administer antibiotic and
corticosteroid as prescribed.
 Maintain normal LOC. Assess level of concsciousness using
pediatric Glasglow coma scale ; assess for signs of cerebral
edema such as dizziness, headache, irregular breathing, neck
pain, nausea or vomiting ; elevate head in neutral position ;
reorient the client to the environment, as needed, and
administer and monitor anticonvulsants drug levels.
 Decrease anxiety. Encourage to express concerns and ask to
express concerns and ask questions regarding the condition of
ill child ; encourage the parent to stay with the child or visit
when able and call when concerned if hospitalized ; assist in
care (hold, feed, bathe, clothe and diaper), and provide
information about child’s daily routines ; encourage to be
involved in care and decision-making regarding needs ; and
clarify any misinformation and answer questions in lay terms
when parents able to listen, give same explanation as other
staff and/or physician gave regarding disease process and
transmission.

VI. PATHOPHYSIOLOGY

Most commonly, bacteria reach the subarachnoid space and meninges

via hematogenous spread. Because white blood cells (WBCs),
immunoglobulins, and complement are normally sparse or absent from
cerebrospinal fluid (CSF), bacteria initially multiply without causing
inflammation.
 I. NAME OF DISEASE

- SEVERE ACUTE RESPIRATORY SYNDROME

II. ETIOLOGY
SARS usually begins with flu-like signs and symptoms — fever,
chills, muscle aches, headache and occasionally diarrhea. After
about a week, signs and symptoms include:

I.Fever of 100.5 F (38 C) or higher

II. Dry cough
III. Shortness of breath

III. DIAGNOSTIC PROCEDURE

Severe Acute Respiratory Syndrome (SARS):

Laboratory diagnostic tests.

29 April 2003

Researchers in several countries are working towards developing fast

and accurate laboratory diagnostic tests for the SARS coronavirus
(SARS-CoV). However, until standardized reagents for virus and
antibodies detection are available and methods have been adequately
field tested, SARS diagnosis remains based on the clinical and
epidemiological findings: acute febrile illness with respiratory
symptoms not attributed to another cause and a history of exposure to
a suspect or probable case of SARS or their respiratory secretions and
other bodily fluids.

Those requirements are reflected in the current WHO case definitions

for suspect or probable SARS. However in several countries (Canada,
France, Germany, Hong Kong SAR, Italy, Japan, the Netherlands,
Singapore, United Kingdom and the United States of America) samples
from suspected and probable SARS cases are being tested for SARS-
CoV. Laboratory test result criteria for confirming or rejecting the
diagnosis of SARS remain to be defined.

1. Molecular tests (PCR)

Polymerase chain reaction (PCR) can detect genetic material of the
SARS-CoV in various specimens (blood, stool, respiratory secretions or
body tissues Sampling for Severe Acute Respiratory Syndrome (SARS)
diagnostic tests). Primers, which are the key pieces for a PCR test, have
been made publicly available by WHO network laboratories on the
WHO web site. A ready-to-use PCR test kit containing primers and
positive and negative control has been developed. Testing of the kit by
network members is expected to quickly yield the data needed to
assess the test’s performance, in comparison with primers developed
by other WHO network laboratories and in correlation with clinical and
epidemiological data.

Principally, existing PCR tests are very specific but lack sensitivity. This
means that negative tests cannot rule out the presence of the SARS
virus in patients. Furthermore, contamination of samples in
laboratories in the absence of laboratory quality control can lead to
false positive results.

Positive PCR results, with the necessary quality control procedures in

place. Recommendations for laboratories testing for SARS-coronavirus,
are very specific and mean that there is genetic material (RNA) of the
SARS-CoV in the sample. This does not mean that there is live virus
present, or that it is present in a quantity large enough to infect
another person.

Negative PCR results do not exclude SARS. SARS-CoV PCR can be

negative for the following reasons:
- The patient is not infected with the SARS coronavirus; the illness is
due to another infectious agent (virus, bacterium, fungus) or a non-
infectious cause.

- The test results are incorrect (“false-negative”). Current tests need to

be further developed to improve sensitivity.

- Specimens were not collected at a time when the virus or its genetic
material was present. The virus and its genetic material may be present
for a brief period only, depending on the type of specimen tested.

2. Antibody tests

These tests detect antibodies produced in response to the SARS

coronavirus infection. Different types of antibodies (IgM and IgG)
appear and change in level during the course of infection. They can be
undetectable at the early stage of infection. IgG usually remains
detectable after resolution of the illness.

The following test formats are being developed, but are not
commercially available yet:

- ELISA (Enzyme Linked ImmunoSorbant Assay): a test detecting a

mixture of IgM and IgG antibodies in the serum of SARS patients yields
positive results reliably at around day 21 after the onset of illness.

– IFA (Immunofluorescence Assay): a test detecting IgM antibodies in

serum of SARS patients yields positive results after about day 10 of
illness. This test format is also used to test for IgG. This is a reliable test
requiring the use of fixed SARS virus on an immunofluorescence
microscope.
Positive antibody test results indicate a previous infection with SARS-
CoV. Seroconversion from negative to positive or a four-fold rise in
antibody titre from acute to convalescent serum indicates recent
infection.

Negative antibody test results: No detection of antibody after 21 days

from onset of illness seems to indicate that no infection with SARS-CoV
took place.

3. Cell culture

Virus in specimens (such as respiratory secretions, blood or stool) from

SARS patients can also be detected by inoculating cell cultures and
growing the virus. Once isolated, the virus must be identified as the
SARS virus with further tests. Cell culture is a very demanding test, but
currently (with the exception of animal trials) only means to show the
existence of a live virus.

Positive cell culture results indicate the presence of live SARS-CoV in

the sample tested.

Negative cell culture results do not exclude SARS (see negative PCR test
result).
IV. MEDICAL MANAGEMENT

Currently, no definitive medication protocol specific to SARS has been

developed, although various treatment regimens have been tried
without proven success. [ 11, 12] The CDC recommends that patients
suspected of or confirmed as having SARS receive the same treatment
that would be administered if they had any serious, community-
acquired pneumonia.

V. NURSING INTERVENTION

Confirmed or suspected cases of SARS should be isolated with airborne,

droplet, and contact precautions and aggressive hospital treatment is
required (Chan, Tang, & Hui, 2006). Although there is no proven
effective treatment for SARS, patients with confirmed or suspected
cases usually receive the same treatment to patients who have been
diagnosed with community-acquired pneumonia (Chan et al, 2006).
VI. PATHOPHYSIOLOGY

The most publicized human coronavirus, SARS-CoV which causes SARS,

has a unique pathogenesis because it causes both upper and lower
respiratory tract infections and can also cause gastroenteritis.
Coronaviruses are believed to cause a significant percentage of all
common colds in human adults.
PANDEMIC DISEASES
I. NAME OF DISEASE

- Spanish Flu Pandemic

II. ETIOLOGY

It was caused by an H1N1 virus with genes of avian origin. Although

there is not universal consensus regarding where the virus originated, it
spread worldwide during 1918-1919. In the United States, it was first
identified in military personnel in spring 1918.
III. DIAGNOSTIC PROCEDURE

Diagnostic tests available for influenza include viral culture, serology,

rapid antigen testing, reverse transcription polymerase chain reaction
(RT-PCR), immunofluorescence assays, and rapid molecular assays.

IV. MEDICAL MANAGEMENT

Treatment is largely supportive and consists of bedrest, increased fluid

consumption, cough suppressants, and antipyretics and analgesics (eg,
acetaminophen, nonsteroidal anti-inflammatory drugs) for fever and
myalgias. Severe cases may require intravenous hydration and other
supportive measures. Antiviral agents may also be considered for
treatment or prophylaxis.

V. NURSING INTERVENTION

The major nursing care planning goals for influenza are: Patient will
achieve and maintain a patent airway. Patient will achieve and maintain
normal respiratory pattern and rate, with no adventitious breath
sounds to auscultation. Patient will achieve and maintain a normal
temperature.

VI. PATHOPYSIOLOGY

Influenza virus affects the respiratory tract by direct viral infection or by

damage from the immune system response. In humans, the respiratory
epithelium is the only site where the hemagglutinin (HA) molecule is
effectively cleaved, generating infectious virus particles. Virus
transmission occurs through a susceptible individual’s contact with
aerosols or respiratory fomites from an infected individual. The inability
of the lung to perform its primary function of gas exchange can result
from multiple mechanisms, including obstruction of the airways, loss of
alveolar structure, loss of lung epithelial integrity from direct epithelial
cell killing, and degradation of the critical extracellular matrix.

Approximately 30–40% of hospitalized patients with laboratory-

confirmed influenza are diagnosed with acute pneumonia. These
patients who develop pneumonia are more likely to be < 5 years old, > 
65 years old, Caucasian, and nursing home residents; have chronic lung
or heart disease and history of smoking, and are immunocompromised.

Influenza can primarily cause severe pneumonia, but it can also present
in conjunction with or be followed by a secondary bacterial infection,
most commonly by Staphylococcus aureus and Streptococcus
pneumoniae. Influenza is associated with a high predisposition to
bacterial sepsis and ARDS. Viral infections presenting concurrently with
bacterial pneumonia are now known to occur with a frequency of 30–
50% in both adult and pediatric populations. The H3N2 subtype has
been associated with unprecedented high levels of intensive care unit
(ICU) admission.

Influenza A is the predominant viral etiology of acute respiratory

distress syndrome (ARDS) in adults. Risk factors independently
associated with ARDS are age between 36 and 55 years old, pregnancy,
and obesity, while protective factors are female sex, influenza
vaccination, and infections with Influenza A (H3N2) or Influenza B
viruses.

In the ICU, particularly during the winter season, influenza should be

suspected not only in patients with typical symptoms and
epidemiology, but also in patients with severe pneumonia, ARDS, sepsis
with or without bacterial co-infection, as well as in patients with
encephalitis, myocarditis, and rhabdomyolysis.

I. NAME OF DISEASE
HIV/AIDS

II. ETIOLOGY

 AIDS is caused by HIV, a human retrovirus.

 Two types – HIV I and HIV II which are genetically different but has
related forms.
 HIV I is most common type associated with AIDS in US, Europe
and Central Africa.
 HIV II causes similar disease in West Africa and India.
 HIV II is transmitted less efficiently than HIV I.

III. DIAGNOSTIC PROCEDURE

An HIV test is used to determine if you have been infected with the
human immunodeficiency virus (HIV). While the test is commonly
performed on a blood or saliva sample, a newer urine-based test was
approved for use in the United States in 2015. While both point-of-care
and at-home testing options are extremely accurate if used correctly,
they can return a false-negative result if you test too soon after an
exposure.

IV. MEDICAL MANAGEMENT

The treatment of HIV/AIDS with medicines is called antiretroviral

therapy (ART). It is recommended for everyone who has HIV. The
medicines do not cure HIV infection, but they do make it a manageable
chronic condition. They also reduce the risk of spreading the virus to
others.
HIV/AIDS medicines reduce the amount of HIV (viral load) in your body,
which helps by :

 Giving your immune system a chance to recover. Even though

there is still some HIV in your body, your immune system should
be strong enough to fight off infections and certain HIV-related
cancers.
 Reducing the risk that you will spread HIV to others.

V. NURSING INTEVENTION

Nursing Interventions Rationale

Lesions of the mouth, throat, and

esophagus (often caused by
candidiasis, herpes simplex, hairy
leukoplakia, Kaposi’s sarcoma other
Assess patient’s ability to chew, taste,
cancers) and metallic or other taste
and swallow.
changes caused by medications may
cause dysphagia, limiting patient’s
ability to ingest food and reducing
desire to eat.

Auscultate bowel sounds. Hypermotility of intestinal tract is

common and is associated with
vomiting and diarrhea, which may
affect choice of diet/route. Lactose
intolerance and malabsorption
(with CMV, MAC, cryptosporidiosis)
Nursing Interventions
Weigh as indicated. Evaluate weight
in terms of premorbid weight.
Compare serial weights and
anthropometric measurements.
Note drug side effects.
Plan diet with patient and include SO,
suggesting foods from home if
appropriate. Provide small, frequent
meals and snacks of nutritionally
dense foods and non acidic foods and
beverages, with choice of foods
palatable to patient. Encourage high-
Rationale
contribute to diarrhea and may
necessitate change in diet or
supplemental formula.
Indicator of nutritional adequacy of
intake. Because of depressed
immunity, some blood tests
normally used for testing nutritional
status are not useful.
Medications used can have side
effects affecting nutrition. ZDV can
cause altered taste, nausea and
vomiting; Bactrim can
cause anorexia, glucose intolerance
and glossitis; Pentam can cause
altered taste and smell; Protease
inhibitors can cause elevated lipids,
blood sugar increase due
to insulin resistance.
Including patient in planning gives
sense of control of environment and
may enhance intake. Fulfilling
cravings for noninstitutional food
may also improve intake. In this
population, foods with a higher fat
content may be recommended as
Nursing Interventions Rationale

calorie and nutritious foods, some of

which may be considered appetite
tolerated to enhance taste and oral
stimulants. Note time of day when
intake.
appetite is best, and try to serve
larger meal at that time.

Limit food(s) that induce nausea

and/or vomiting or are poorly
Pain in the mouth or fear of
tolerated by patient because of
irritating oral lesions may cause
mouth sores or dysphagia. Avoid
patient to be reluctant to eat. These
serving very hot liquids and foods.
measures may be helpful in
Serve foods that are easy to swallow
increasing food intake.
like eggs, ice cream, cooked
vegetables.

Schedule medications between meals

(if tolerated) and limit fluid intake Gastric fullness diminishes appetite
with meals, unless fluid has and food intake.
nutritional value.

Encourage as much physical activity as May improve appetite and general

possible. feelings of well-being.

Reduces discomfort associated with

Provide frequent mouth care,
nausea and vomiting, oral lesions,
observing secretion precautions.
mucosal dryness, and halitosis.
Avoid alcohol-containing
Clean mouth may enhance appetite
mouthwashes.
and provide comfort.
Nursing Interventions
Provide rest period before meals.
Avoid stressful procedures close to
mealtime.
Remove existing noxious
environmental stimuli or conditions
that aggravate gag reflex.
Encourage patient to sit up for meals
Record ongoing caloric intake.
Maintain NPO status when
appropriate.
Insert or maintain nasogastric (NG)
tube as indicated.
Administer medications as indicated:
 Antiemetics: prochlorperazine
Rationale
Minimizes fatigue; increases energy
available for work of eating and
reduces chances of nausea or
vomiting food.
Reduces stimulus of the vomiting
center in the medulla.
Facilitates swallowing and reduces
risk of aspiration.
Identifies need for supplements or
alternative feeding methods.
May be needed to reduce nausea
and vomiting.
May be needed to reduce vomiting
or to administer tube feedings.
Esophageal irritation from existing
infection (Candida, herpes, or KS)
may provide site for secondary
infections and trauma;
therefore, NG tube should be used
with caution.
Reduces incidence of nausea and
Nursing Interventions
(Compazine), promethazine
(Phenergan),
trimethobenzamide (Tigan)
 Sucralfate (Carafate)
suspension; mixture of Maalox,
diphenhydramine (Benadryl),
and lidocaine (Xylocaine);
 Vitamin supplements
 Appetite stimulants: dronabinol
(Marinol),  megestrol (Megace),
oxandrolone (Oxandrin)
 TNF-alpha inhibitors:
Rationale
vomiting, possibly enhancing oral
intake.
Given with meals (swish and hold in
mouth) to relieve mouth pain,
enhance intake. Mixture may be
swallowed for presence of
pharyngeal or esophageal lesions.
Corrects vitamin deficiencies
resulting from decreased food
intake and/or disorders of digestion
and absorption in the GI
system. Avoid megadoses and
suggested supplemental level is two
times the recommended daily
allowance (RDA).
Marinol (an antiemetic)
and Megace (an antineoplastic) act
as appetite stimulants in the
presence of AIDS. Oxandrin is
currently being studied in clinical
trials to boost appetite and
improve muscle mass and strength.
Reduces elevated levels
Nursing Interventions Rationale

of tumor necrosis factor (TNF)

present in chronic illness
thalidomide; contributing to wasting or cachexia.
Studies reveal a mean weight gain
of 10% over 28 wk of therapy.

Inhibit GI motility subsequently

 Antidiarrheals:  diphenoxylate
(Lomotil), loperamide
(Imodium), octreotide
(Sandostatin);
decreasing diarrhea. Imodium or
Sandostatin are effective
treatments for secretory diarrhea
(secretion of water and electrolytes
by intestinal epithelium).

 Antibiotic therapy: ketoconazole May be given to treat and prevent

(Nizoral), fluconazole (Diflucan). infections involving the GI tract.

VI. PATHOPHYSIOLOGY

Pathology of AIDS

HIV infection passes through a series of steps or stages before it turns

into AIDS. These stages of infection as outlined in 1993 by the Centers
for Disease Control and prevention are:
 1. Seroconversion illness – this occurs in 1 to 6 weeks after acquiring
the infection. The feeling is similar to a bout of flu.

2. Asymptomatic infection – After seroconversion, virus levels are

low and replication continues slowly. CD4 and CD8 lymphocyte
levels are normal. This stage has no symptoms and may persist for
years together.

3. Persistent generalised lymphadenopathy (PGL) – The lymph nodes

in these patients are swollen for three months or longer and not
due to any other cause.

4. Symptomatic infection – This stage manifests with symptoms. In

addition, there may be opportunistic infections. This collection of
symptoms and signs is referred to as the AIDS-related complex
(ARC) and is regarded as a prodrome or precursor to AIDS.

5. AIDS – this stage is characterized by severe immunodeficiency.

There are signs of life-threatening infections and unusual
tumours. This stage is characterized by CD4 T-cell count below
200 cells/mm3.

6. There is a small group of patients who develop AIDS very slowly,

or never at all. These patients are called nonprogressors.

The pathological spectrum of HIV infection is changing as the infection

spreads into new communities with different potential opportunistic
diseases, and as medical science devises drugs against HIV replication.

Geographical pathology of HIV/AIDS

Genetics and geographical location has a role in the pattern of

opportunistic infections. A second determinant is the speed of decline
in the immune system. Many of the opportunistic infections are of low
virulence and are only encountered if patients survive with low CMI.

Genetics and earlier site of stay also plays a role. For example, African
HIV-infected patients reside in the UK have high rates of tuberculosis
and this is usually a reactivation of latent infection acquired in the
country of origin.

Some opportunistic infections include;

Viral infections

 Cytomegalovirus (CMV)

 Herpes simplex

 Molluscum contagiosum

 Herpes zoster

 Measles

 Human papilloma virus (HPV)

 Human herpes virus 8 (HV8)

 Epstein-Barr virus (EBV)

Bacterial infections

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 Recurrent bacterial pneumonia (commonly Streptococcus

pneumoniae)

 Mycobacterium tuberculosis

 Non-tuberculosis mycobacteriosis (particularly M. avium-

intracellulare complex)

 Systemic non-typhoid Salmonella infections* (notably S.

enteritidis and S. typhimurium)

 Pseudomonas spp. septicaemia and `vasculitis'

 Bartonella spp. (causing bacillary angiomatosis)

 Rhodococcus equi

 Nocardia spp.

Fungal infections

 Candida severe infection

 Pneumocystis jiroveci pneumonia

 Cryptococcus neoformans

 Histoplasma capsulatum

 Coccidioides immitis

 Aspergillus spp.

 Penicillium marneffei
  Protozoal infections

 Toxoplasma gondii

 Cryptosporidium parvum

 Isospora belli

 Leishmania spp.

 Microsporidia spp. (commonly Encephalitozoon intestinalis,

Enterocytozoon bieneusi)

 Acanthamoeba spp.

 Trypanosoma cruzi

Tumours

 Kaposi's sarcoma

 Primary cerebral lymphoma

 High-grade non-Hodgkin lymphoma

 Carcinoma (invasive) of the cervix

 Carcinoma of the conjunctiva

 Carcinoma of the anus

 T-cell lymphoma

 Hodgkin's disease

 Lymphoproliferative disease, pre-lymphomatous

Other conditions
 HIV-wasting syndrome (fever, weight loss, diarrhoea)

 HIV-associated dementia or memory loss

 Various dermatitis patterns (e.g. pruritic rash, eosinophilic

folliculitis)

 Skeletal myopathy

 Peripheral and autono

 Peripheral and autonomic neuropathy

 Cardiomyopathy

 Pulmonary hypertension

 Vasculitis

 HIV-associated nephropathy (HIVAN)

 Haemolytic uraemic syndrome (HUS) and thrombotic

thrombocytopaenic purpura (TTP)

 Oral and oesophageal ulcers

 Dyshaemopoiesis and marrow serous atrophy

 SPORADIC DISEASES

I. NAME OF DISEASE

TYPHOID FEVER
II. ETIOLOGY

Typhoid fever is caused by Salmonella enterica serotype Typhi bacteria.

Typhoid fever is contracted by the ingestion of contaminated food or
water. Diagnosis of typhoid fever is made when Salmonella bacteria are
detected with stool, urine, or blood cultures.

III. DIAGNOSTIC PROCEDURE

For the culture, a small sample of your blood, stool, urine or bone
marrow is placed on a special medium that encourages the growth of
bacteria. The culture is checked under a microscope for the presence of
typhoid bacteria. A bone marrow culture often is the most sensitive test
for Salmonella typhi.
Although performing a culture test is the most common diagnostic test,
other testing may be used to confirm a suspected typhoid fever
infection, such as a test to detect antibodies to typhoid bacteria in your
blood, or a test that checks for typhoid DNA in your blood.

IV. MEDICAL MANAGEMENT

Antibiotics are used to treat typhoid fever. These medications kill the
bacteria that cause the infection. Several different types of antibiotics
are used to treat typhoid fever. In many cases, typhoid fever is treated
with ampicillin, chloramphenicol, or cotrimoxazole (Bactrim®).
However, doctors also use fluoroquinolones (including Cipro® and
Levaquin®), cephalosporins (including Cefepime®), and azithromycin.

Your doctor will choose based on the most up-to-date

recommendations. Antibiotics are widely available in the United States
and in most other countries in the world. Do not attempt to self-treat
with leftover antibiotics.

Some people need supportive therapies, such as fluid or electrolyte

replacement, depending on the severity of the infection.

V. NURSING INTERVENTION

 Provide assistance for ADLs. Provide assistance to meet their

daily needs; involve the family in the fulfillment of ADL; and
 explain the purpose of bed rest to prevent complications and
speed up the healing process.

 Encourage increase in fluid intake. Monitor the status of

hydration as needed; monitor the fluid intake daily; encourage an
increase in fluid intake; and collaborate with other medical team
for IV fluid administration.

 Improve nutritional intake. Monitor the amount of caloric intake;

monitor weight loss; provide a comfortable environment during
meals; and encourage an increase in protein and vitamin C intake
to meet nutritional needs.

 Reduce or diminish pain. Assess the level of pain, location,

duration, intensity, and characteristics; provide warm compresses
on areas with pain; and administer analgesics as prescribed.

 Improve body temperature. Monitor patient temperature degree

and patterns; observe for chills and profuse diaphoresis; provide
tepid sponge baths and avoid the use of ice water and alcohol;
and administer antipyretics as prescribed.

VI. PATHOPHYSIOLOGY

All pathogenic Salmonella species, when present in the gut are engulfed
by phagocytic cells, which then pass them through the mucosa and
present them to the macrophages in the lamina propria.

 Salmonella 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.

 Typhoidal salmonella co-opt the macrophages’ cellular machinery

for their own reproduction as they are carried through the
mesenteric lymph nodes to the thoracic duct and the lymphatics
and then through to the reticuloendothelial tissues of the liver,
spleen, bone marrow, and lymph nodes.

 Once there, they pause and continue to multiply until some

critical density is reached; afterward, the bacteria induce
macrophage apoptosis, breaking out into the bloodstream to
invade the rest of the body.

 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.

I. NAME OF DISEASE

Sporadic late-onset nemaline myopathy, or SLONM

II. ETIOLOGY

Sporadic late-onset nemaline myopathy, or SLONM, is a very rare

disease, one of the nemaline myopathies, causing loss of muscle bulk
and weakness in the legs but sparing the cranial nerves, and beginning
its clinical course after age 40. It was first identified in 1966 at the Mayo
Clinic, by A.G. Engel, and that same year W.K. Engel and J.S. Resnick
noted another case that they elaborated in 1975. The diagnosis of the
disease rests on subacutely evolving weakness after age 40, normal to
low CK level, a myopathic EMG with fibrillations, and often a
monoclonal gammopathy. The diagnosis is confirmed by visualizing
rods in cryosections on light and electron microscopy. The associated
monoclonal gammopathy has an unfavorable prognosis.

III. DIAGNOSTIC POCEDURE

The myopathic EMG demonstrates fibrillation potentials. The serum CK

level will be normal or low normal. The muscle biopsy will demonstrate
the nemaline rods, but as they are less than 1 µm in length they are
easily overlooked. The sections must be trichromatically stained and
sectioned at a thickness of 2 to 4 µm for effective visualization.
Immunostains for myotilin and α-actinin all but clinch the diagnosis.
However, nemaline rods may still be visible post-mortem in
neurosarcoidosis, which may remain on the differential. Generally the
outcome is grim, with respiratory insufficiency the cause of death.

IV. MEDICAL MANAGEMENT

Rehabilitation for muscle strengthening can be useful in alleviating

symptoms. Improvement has been noted in two HIV-negative
individuals treated with immunoglobulin (IViG) agents. Improvement
has also been noted with autologous stem cell transplantation, and
chemotherapy with melphalan.

V. NURSING INTERVENTION
Intravenous methylprednisolone (1000mg/day for 3 consecutive days
x2) was administered, resulting in a dramatic improvement in the
proximal muscle weakness and the symptoms

VI. PATHOPHYSOLOGY

The etiology is unknown. Some cases of SLONM have been comorbid

with HIV infection, and others with immune disorders, and so both a
viral trigger and an autoimmune disorder have been considered
candidate etiologies. The monoclonal gammopathy of unknown
significance (MGUS) associated with a worse prognosis also argues for
an immune disorder. On electron microscopy, nemaline bodies within
the affected muscle fibers may be found. These bodies are sometimes
crisply rod-shaped, but can also be irregular and punctate. The rods
may be found alongside atrophic muscle fibers, and may be seen arising
from the thickened Z-discs of the sarcolemmae. Affected fibers may be
vacuolated or lobulated.