PBL 1 SESSION 1

GROUP 12
PREPARED BY
1) AHMAD DANIEL LIAW BIN ISMAIL (2210461)
2) ADLINA BINTI MOHAMAD KAMAL (2217658)
3) ILYA ILHAMI ZUHDI BINTI MOHAMAD ZAINI (2212676)
4) MUHAMMAD AZFAR FATHI BIN MAT ZAID (2216795)
5) MUHAMMAD FAIZ IZUDDIN BIN BADARULLAH (2219157)
6) MUHAMMAD IZZAT HAKIMI BIN AZLAN (2211507)
7) NAFEESA SYAZANA BINTI MOHD FAIRUZ FADLY (2211668)
8) NUR FAISYA DIANA BINTI SUHAIMI (2213738)
9) NUR HAIFA AYUNI BINTI ALI (2114740)
10) SYARAH AISYA BINTI MUHD SABRI (2218886)
11) WAN NURHANAN AQILAH BINTI WAN HANAPI (2217428)
CASE SUMMARY
Age:35 y/o
Gender:Female
HOPI
Fever
- persistent(3 months) fever and chills
-fever not alleviated by taking drugs and worsened over 2 days bfr admission .

Diarrhoea
chronic diarrhoea (3 months) nad become more frequent.
Frequency:4-5 times. Yet, it increased in last two weeks .

Others :
having difficulty of breathing for the past few days (unproductive cough)
-Covid-19 antigen test- -ve
-no headache, no ear discharge,no urinary symptoms
-slight creamy-white itchy vaginal discharge .
-lost 10 kgs in last 3 months (45 kg)
CASE SUMMARY
HISTORY
-No significant past medical and family history.
-Social-Husband is an intravenous drug user (ivu)
-Has 2 children with the previous husband. Both are well. She gave a history of two
abortions with her current spouse who married about 10 years ago.
-She is a non-smoker and denied dependence on drugs.
CASE SUMMARY
CASE SUMMARY
CASE SUMMARY
CASE SUMMARY
 RESPIRATORY
SYSTEM
EXAMINATION

BY ILYA ILHAMI ZUHDI BINTI

MOHAMAD ZAINI (2212676)

Source: Talley and O'Connor's Clinical Examination

 Step 1: Introduce Yourself
Name
Year
University

Step 2: Confirm Patient Details Step 3: Explain Examination

Tell your purpose and what parts of the
Patient's name
Date of birth assessment will be involved.

Step 5: General Examination

Step 4: Gain Consent
Treatment around the bad
Ask the permission Cyanosis
Ask the patient if they have any pain SOB
anywhere. Cough
Ask if they have any questions (examination). Wheeze or Stridor
Cachexia
 Step 6: Inspect Hand
Peripheral cyanosis
Bruising/thinned skin(Long term steroid use)
Tar staining (smoker)
Finger clubbing
Temperature
Fine Tremor
Asterixis
Assess rate (Normal: 12-20 breaths per minute)

Step 7: Assess Jugular Venous

Ask the patient to turn their head to the left. Step 8: Inspect Face
Located between two heads of the
Inspect for central cyanosis (hypoxia)
sternocleidomastoid.
Conjunctival pallor (anaemia).
Raised in cor pulmonale.( Right-sided heart
failure)

Step 9: Inspect Mouth

Step 10: Inspect the chest
Angular stomatitis/cheilitis.
Central cyanosis. Chest wall deformities.
Scars.
 Step 11: Inspect Scars
Central chest (sternotomy and thoracotomy)
Clavicular (pacemaker)
Mid axillary (Chest drain)
Lateral (Lateral Thoracotomy)

Step 12: Assess Tracheal position and

Cricosternal Distance Step 13: Palpate Apex Beat
Tell the patient you want to feel the position
Normal= Fifth intercostal space mid-
of the windpipe. (Normal: along the center of
clavicular line
the throat)
Normal= 3-4 fingers.

Step 14: Assess Chest Expansion Step 15: Percuss the Lung fields
Resonant percussion (normal)
Reduce chest expansion
Dull Percussion
- Lung collapse
- Consolidation
- Pneumonia
- Collapse
- Effusion
Note cardiac dullness (right ventricular dilation)
 Step 16: Auscultate the Lung Fields
Vesicular breathing (Normal)
Inspiratory stridor ( Upper airway obstruction)
Wheeze (asthma and COPD)
Coarse and Crackles ( Pneumonia and pulmonary
oedema)
Fine Crackles (Pulmonary fibrosis)

Step 17: Assess Vocal Resonance

Step 18: Palpate Lymph Nodes
By using tactile vocal fremitus (say 99)
The patient needs to sit forward to us.
Increased vocal resonance ( consolidation,
Check lymphadenopathy
lobar collapse, tumour)
Causes: Infection, Malignancy, Sarcoidosis
Decreased vocal resonance ( Pleural effusion)

Step 19: Inspect the Posterior Chest Wall by Step 20: Percuss the Posterior Chest Wall
assessing posterior chest expansion.
Resonant ( Normal)
Unilaterally reduced chest expansion Dullness ( consolidation/ collapse)
- Lung collapse Stony Dulness ( Pleural effusion)
- Pneumonia Hyper- resonant ( Pneumathorax)
 Step 21: Auscultate the Posterior Chest Wall
Vesicular breathing (Normal)
Inspiratory stridor ( Upper airway obstruction)
Wheeze (asthma and COPD)
Coarse and Crackles ( Pneumonia and pulmonary
oedema)
Fine Crackles (Pulmonary fibrosis)

Step 22: Assess Vocal Resonance Step 23: Palpate for Sacral and Pedal
By using tactile vocal fremitus (say 99) Oedema.
Increased vocal resonance ( consolidation,
Press on the patient's lower back
lobar collapse, tumour)
Pedal Oedema ( Right ventricular failure)
Decreased vocal resonance ( Pleural effusion)

Step 25: Thanks the Patient and Summarize

Step 24: Assess for signs of DVT Findings.
Proven when the patient has pain in the Trachea was centrally located. Chest expansion was
calves during the press. slightly diminished and bilateral generalized
crepitations (crackles) were heard on auscultation.
 R H A N AN
WAN N U
AQ I LA H
22 17 4 28
R R H OE A
D IA S)
& C A US E
(TY P ES

Reference:
1. Vinay Kumar, Abul K. Abbas, Jon C. Aster, (2018) Robbins Basic Pathology, Tenth Edition, Elsevier Inc.
2. Gary D. Hammer, Stephen J. McPhee, (2019) Pathophysiology of Disease: An Introduction to Clinical Medicine,
Eight Edition, McGraw-Hill Education.
 Diarrhoea
an increase in stool mass, frequency, or
fluidity (> 200 g / day)
 Types of Diarrhoea
1. Secretory diarrhoea
1.
rate of fluid secretion from
epithelial cells into GI tract
lumen exceeds rate of
absorption.
2. Osmotic diarrhoea
increase amounts of poorly
absorbable, osmotically active
solutes
cause sodium & water influx into
bowel lumen
3. Exudative diarrhoea
exudation of mucous, blood &
Inflammatory protein from inflammatory sites
into bowel lumen
increase osmotic load
water move across epithelium
Watery
4. Malabsorptive
diarrhoea
malabsorption of nutrients &
Fatty steatorrhoea
stools : fatty, pale-coloured,
extremely smelly & difficult to flush
steatorrhoea = presence of > 7g fat
in a 24-hour stool collection
Causes of diarrhoea
Secretory diarrhoea Osmotic diarrhoea

enterotoxins: Lactose intolerance:

produced by Vibrio cholerae, etc lack of lactase
increase chloride permeability osmotically active lactose remain in lumen.

congenital defects:
lining of intestine is different from normal Magnesium antacids:
intestine Magnesium stimulates muscle contraction
can secrete but can't absorbe large amount of salt high dose of Mg antacid --> diarrhoea
from intestine

hormonal condition:
hormones of tumour origin interact with small
intestinal mucosa
prevent absorption of sodium, chloride & water in
intestines
Causes of diarrhoea
Exudative Malabsorptive
diarrhoea diarrhoea

pancreatic disease:
e.g pancreatitis, pancreatic cancer &
Inflammatory bowel disease (Crohn's disease
cystic fibrosis
& ulcerative colitis):
impair production & secretioon of
lining of intestine inflame
digestive enzymes (lipase)
can't absorb all fluid
fats & other nutrients can't be broken
down & can't be absorbed

Infection:
e.g bacterium Shigella
Shigella infection --> more severe &
difficult to treat in HIV patient
due to weakened immune system by HIV
 A Y U N I
H A I F A
NUR ( 2 1 1 4 7 4 0 )
I A L I
B IN T
UN IS TI C
OPPO R T
O NS A N D
IN FE CT I SES
D D IS EA
S OC IA TE
AS
Opportunistic infections
infections occurring due to bacteria, fungi, viruses, or parasites that normally do not cause
disease in a healthy individual, but become pathogenic when the body's defense system is impaired
can also be represented by unusually severe infections caused by common pathogens
found in patients with:
malignancy
immunosuppressive therapy
AIDS
burns
dialysis patients
diabetes
 Opportunistic mycosis
Candidiasis
caused by candida spp. (eg: c. tropicalis, c.
glabrata, c. parapsilosis, c, krusei)
yeast like infection causing mucocutaneous,
cutaneous and systemic infections
Cryptococcosis
yeast infection caused by cryptococcus spp. (eg: cr.
neoformans, cr. gattii, cr. albidus, cr. laurentii
if spread to CNS can cross BBB
called as trojan horse inside macrophage
clinical manifestations: skin infection, respiratory
pneumonitis, meningitis, meningoencephalitis,
cutaneous lesions and bone infection
Penicilliosis
caused by penicillium spp. (eg: penicillium marneffei)
causes skin lessions and disseminated infections
Aspergillosis
systemic and superficial fungal infection caused by
aspergillus spp. (eg: a. fumigatus, a. niger, a. flavus)
clinical manifestations: lung infection (allergic
aspergillosis, aspergilloma, invasive aspergillosis). CNS
infection, keratomycosis, paranasal sinus infections.
cutaneous infections, endocarditis
Zygomycosis (mucormycosis)
caused by aseptate filamentous fungi (eg: Rhizopus
spp. Mucor spp. and Lichtheimia spp.)
clinical manifestations: rhinocerebral, pulmonary,
cutaneous, GIT, disseminated zygomycosis
Pneumocystosis
caused by pneumocystis carinii and pnemocystis jiroveciii
clinical manifestations: primary atypical pneumonia,
extrapulmonary pneumocystosis)
Opportunistic bacteriosis Bartonellosis
caused by bartonella spp. (eg: b. henselae, b.
Salmonellosis
quintana, b. bacilliformis)
caused by salmonella spp, (s. enterica and
clinical manifestations: cutaneous lesions,
s. bongori)
subcutaneous nodules, osteomyelitis, bacillary
clinical manifestations: gastroenteritis,
peliocis hepatitis, disseminated infection, and
bacteremia, focal salmonella infection
systemic symptoms of fever, night sweats, and
weight loss
Staphylococcosis and streptococcosis
caused by staphylococcus spp. and Tuberculosis
streptococcus spp. (eg: staph. aureus and caused by mycobacterium tuberculosis
strep. pneumoniae) clinical manifestations: reactivation of latent
clinical manifestations: pneumonia, sinusitis, infection-active pulmonary tuberculosis,
skin-soft tissue infection, if spread to blood- bacteremia-spread to other organs causing
bacteremia, osteomyelitis/arthritis, meningitis disseminated TB or miliary TB

NTM infection
caused by nontuberculosis mycobacteria (eg: m. avium, m. kansasii)
clinical manifestations: extrapulmonary disease, bacteremia
 Opportunistic virosis
CMV infection
caused by cytomegalovirus(CMV)
clinical manifestations: pneumonia, colitis, CNS disease,
hepatitis, retinitis, nephritis, myocarditis, pancreatitis
EBV infection
caused by epstein-barr virus
clinical manifestations: fever, lymphadenitis, pharyngitis,
lymphadenopathy, hepatosplenomegaly, extensive tissue
damage-liver n bone marrow, jaundice
HBV infection
caused by hepatitis B virus
clinical manifestations: abdominal pain, nausea, vomiting,
fever, arthralgias, with or without jaundice, chronic
infections-15-40% develop cirrhosis hepatocellular
carcinoma or liver failure
Influenza
caused by influenza virus
clinical manifestations: pneumonia, encephalitis
HEV infection
caused by hepatitis E virus
clinical manifestations: chronic hepatitis
HSV infection
caused by herpes simplex virus
clinical manifestations: chronic ulcers-orolabial, cutaneous or
genital, pneumonitis or esophagitis, encephalitis or other
visceral involvement
VZV infection
caused by varicella-zoster virus
clinical manifestations:
varicella: neurologic- encephalitis, ataxia, transverse myelitis),
hepatitis, pneumonia, multiorgan failure with disseminated
intravascular coagulation. primary chronic infection: lesions
evolve into nonhealing ulcers or necrotic, crusted and
hyperkeratotic, verrucous lesions
herpes zoster: painful cutaneous eruption in a dermatomal
distribution, erythematous maculopapular rash, new vesicles
formation with lesion pustulation and scabbing
Opportunistic parasitosis
Toxoplasmosis
caused by toxoplasma gondii
clinical manifestations: visceral
disseminated, cervical lymphadenopathy,
constitutional symptoms- fever, chills n
sweats, others- myalgias, pharyngitis,
hepatosplenomegaly
Cryptosporidiosis
caused by cryptosporidium parvum or cryptosporidium hominis
clinical manifestations: chronic diarrhea (>1 month)
Giardiasis
caused by giardia
clinical manifestations chronic diarrhea (>1 month)

Leishmaniasis
caused by leshmania spp.
clinical manifestations: reecurrent, atypical visceral leishmania

Trypanosomiasis
clinical manifestations: meningoencephalitis, central nervous
system mass, myocarditis
 A D IANA
AIS Y
NUR F 7 38)
(22 13

L FL ORA
NO RM A
C O M M ON
LIST OF
O BIO TA
MICR

REFERENCES :
1) Murray, P. R., Pfaller, M. A., & Rosenthal, K. S. (2021). Medical
microbiology. Elsevier
2) lippincott`s microbiology
 NORMAL FLORA
population of microorganism that inhabit the skin and mucous
membrane of healthy normal person
or
Microoragnism that are frequently found on or within the body
of healthy person
also termed commensals, which literally means "organism that
dine together"
A healthy newborn acquires normal flora from food and the
environment including from others human
 types of normal flora
resident
relatively fixed types of
microoragnisms regularly
found in a given area at a
given age
example : E.coli in the
intestine of the human
transient
non pathogenic or
potentially pathogenic
microorganism
hours, days or weeks
derived from the
environment
does not establish itself
permanently on the surface
example : Pneumococcus or
meningococcus may be found
in nasopharynx of human
from time to time
NORMALLY STERILE SITES
blood
CSF
Peritoneal fluid
pleural fluid
bone
internal body sites( lymph nodes, brain, heart, liver and spleen)
Joint fluid
distribution of normal flora in the body
skin
resident microflora consists
primarily bacteria and fungi
resident bacteria can be in
any layer of the skin
acquire any transient
bacteria from the
environment but it either get
washed off or die because
skin is dry ,has acidic pH and
produce sweat and oil
skin flora are harmless
if penestrated , it might cause
bloodstream infections
 distribution of normal flora in the body
conjunctiva
mouth
normally held in check by
have both aerobic &
the flow of the tears
anaerobic bacteria
contain antimicrobial
also yeast, moulds ,protozoa
enzyme lysozyme
and viruses can be living in the
help limit the bacterial
mouth
population of the
mouth / oral cavity :
conjunctiva
lactobacilli, staphylococcus,
streptococci, bacteroids
teeth : streptococcus mutants
poor dental hygiene help
bacteria to grow and cause
dental caries, gingivitis
after dental surgery, might be a
risk of blood stream infection
that might cause endocarditis
 intestinal tract distribution of normal urogenital tract
flora in the body the low pH of the adult vagina is
stomach : density of
maintained by the presence
microorganisms relatively
Lactobacillus species
low due to gastric enzmes
population decreased by
acid tolerance antimicrobial drug,
streptococci, pH rises
Helicobacter pylori potential pathogens can
density of organisms overgrow
increases along the
alimentary canal
(contents in ileum and
large intestine)
Escherichia coli, less than
0.1 % of total population
but E. coli is major cause
of urinary tract infection
 FA THI
AZFAR
22167 95

E S OF H IV
RT I
PROPE L O GY O F HIV
PHY SI O
PATHO

SOURCE: ROBBINS PATHOLOGY (M/S:175)

 PROPERTIES OF HIV
LENTIVIRUS FAMILY
SIMIAN
HIV IMMUNODEFICIENCY
FELINE VIRUS
VISNA VIRUS
IMMUNODEFICIENCY
OF SHEEP VIRUS

HIV HAS TWO GENETICALLY DIFFERENT BUT RELATED FORMS

HIV 1 HIV 2
STRUCTURE OF HIV
spherical
contains electron dense, cone-shaped core
surrounded by lipid envelope
the core consists of
major capsid protein p24
nucleocapsid protein p7/p9
2 copies of viral genomic RNA
viral enzymes
(reverse transcriptase,integrase,protease)
viral core is surrounded by a matrix protein
called p17, lying underneath the lipid
envelope
scattered on the lipid envelope are
two viral glycoproteins (gp120,gp41)
 HIV INFECTION
characterized by gradual destruction of T helper Cells
CD4 cells have high affinity for HIV

HIV infects the host by undergoing 7 steps

1. Binding
2. Fusion
3. Reverse Transcription
4. Integration
5. Replication
6. Assembly
7. Budding

HIV binds to CD4,
HIV recognizes CD4 glycoprotein on the HIV
molecule surface (gp120) binds to
coreceptors on CD4
(CXCR4, CCR5)
proviral DNA may be
Newly formed HIV transcribed,
proteins assemble and leading to the expression of
comes together with viral proteins that are
copies of HIV RNA to required
form new immature virion for the formation of
complete viral particles.
the newly formed Loss of CD4+ T cells
immature HIV buds out mainly because of the
cytopathic effect,
of the CD4
leading to
immunodefficiency
syndrome
After fusion, the virus
Conformational change
core containing the
in gp41 (glycoprotein
HIV
on HIV) leading to
genome (RNA) enters
fusion of virus with the
the cytoplasm of the
host cell
cell.
DNA enters the host RNA genome undergoes
nucleus and integrated into reverse transcription
the host genome by the with the help of reverse
enzyme integrase. The transcriptase, forming ds
integrated HIV DNA is DNA of HIV
called provirus
 D FAIRUZ
BINTI MOH
SYAZANA
NAFEESA FADLY

(2211668)

T ION /AIDS R AC T
N FE C AL T
HIV I TIC GEN IT
PPO RT UNIS
O
N R Y T RACT
O
INFECTIO ISTIC RESPIRAT
N
OPPORTU
N
INFECTIO

SOURCE:
ROBBINS PATHOLOGY (M/S: 173 - 175, 256)
WEBSTER'S NEW WORLD MEDICAL DICTIONARY
HTTPS://WWW.MOH.GOV.MY/MOH/RESOURCES/PENERBITAN/LAPORAN/UMUM/20211
130_MYS_COUNTRY_REPORT_2021.PDF
HTTPS://WWW.NCBI.NLM.NIH.GOV/BOOKS/NBK459317/
HTTPS://WWW.WIKIDOC.ORG/INDEX.PHP/CANDIDA_VULVOVAGINITIS_PATHOPHYSI
OLOGY
HTTPS://EMEDICINE.MEDSCAPE.COM/ARTICLE/211316-OVERVIEW#A3
Once HIV infect the host cells, it will produce cellular immune deficiency which
is the depletion of helper T lymphocytes (CD4+).

Acute seroconversion Asymptomatic HIV AIDS

Rapid plasma verimea &
widespread dissemination
of the virus.
Observed 4-11 days after
the mucosal entrance of the
virus. Can take weeks to
months.
Symptoms :
1. fever
2. flu-like illness
3. lymphadenopathy
4. rash
infection Immune system is damaged
Person infected doesn’t enough.
really show any signs or Cannot fight opportunistic
symptoms for years to infection.
decade or more. Diagnosed if the person has
Viral replication is still CD4+ counts <200μL
ongoing but at very low Many OIs are used to mark
level. when HIV infection has
Taking antiretroviral progressed to AIDS.
therapy (ART) will slow
down the progression to
AIDS for a few more
decades.
 A disease caused by the retrovirus human immunodeficiency virus (HIV).
Characterized with profound immunosuppression that leads to opportunistic
infections, secondary neoplasms, & neurologic manifestations. It's the 3rd
stage of HIV infection.

retrovirus? Opportunistic infection?

Virus that is composed of RNA, not DNA.
Has reverse transcriptase giving them the
unique property of transcribing their RNA
into DNA after entering a cell. The retroviral
DNA can then integrate into the
chromosomal DNA of the host cell so that it
can be expressed there.
Infection not typically seen in healthy
person.
Occurs due to one's weakened immune
system.
Danger to people with immunodeficiency or
receiving immunosuppressive drugs.
HIV does not cause death, but the
opportunistic infections due to the effect
of the HIV on immune system can be lethal.
Epidemiology
In USA
In Malaysia
 G
e
n
d
e
r

S
t
A a
g t
e e
 MODES OF TRANSMISSION
Transmission of HIV occurs under conditions that facilitate exchange
of blood or body fluids containing the virus or virus-infected cells.

Sexual transmission Parenteral transmission Mother-to-infant

Dominant mode of
infection worldwide
In homosexual groups, the
virus is carried in the semen
and enters the recipient's
body through abrasions in
rectal or oral mucosa or by
direct contact with mucosal
lining cells.
Transmission is enhanced
by coexisting STD especially
those associated with
genital ulceration.
Occurs in IVDU , transmission
hemophiliacs who received Major cause of paediatric
contaminated factors VIII & AIDS.
IX concentrates, & other Routes :
recipients of contaminated 1. in utero by transplacental
blood products. spread
Occurs by sharing needles, 2. during delivery through an
syringes & other infected canal
paraphernalia 3. after birth by ingestion of
contaminated with HIV- breast milk
containing blood. most common mode is
prepartum & peripartum
transmission.
Typical adult patient with AIDS presents with fever, weight loss,
chronic diarrhoea, multiple opportunistic infections, neurologic
disease & secondary neoplasms.

Opportunistic Opportunistic
Genital Tract Respiratory Tract
Infection Infection
Candidiasis Pneumocytis
Herpes Simplex Virus Toxoplasma
Candidiasis
Cryptococcus
Cytomegalovirus
Histoplasma
Micobacterium
Nocardia
 FAIZ IZUDDIN
PNEUMOCYSTIS CARINII
INFECTION

References:
https://www.ncbi.nlm.nih.gov/books/NBK482370/
https://www.cdc.gov/fungal/diseases/pneumocystis-pneumonia/index.html
https://www.ncbi.nlm.nih.gov/books/NBK8137/
 PNEUMOCYSTIS CARINII PNEUMONIA RISK
-KNOWN AS PNEUMOCYTIS JIROVECI PNEUMONIA (PJP)
-A fungal infection that most commonly affects -Weaken immune system
the immunocompromised and, in some cases, -Taking medicine that lowers the body ability to
can be severely life-threatening fight germ or disease (corticosteroid)
-Common opportunistic infection with persons -Chronic lung diseases
with HIV -Cancer
-Inflammatory diseases or autoimmune diseases
(for example, lupus or rheumatoid arthritis)
-Solid organ or stem cell transplant

Pneumocystis carinii stained with Gomori's methenamine silver nitrate

method
Cysts stain brownish black,spherical, oval, cup-shaped, thick-walled cyst and
measure 4 to 6 μm in diameter.
 CLINICAL MANIFESTATION CHEST X-RAY FINDING
Fever
Cough Can be normal or show perihilar fluffy
Dyspnea shadows or pneumothorax
Fatigue
Chills
Chest Pain
Weight Loss
Tachypnea
50% of patients may present with crackles
and rhonchi on auscultation
 LABARATORY FINDING TREATMENT

LOW CD4 COUNT Pentamidine isethionate

OXYGENATION Trimethoprim-sulfamethoxazole
-The alveolar-arterial oxygen gradient ranging Atovaquone
Mild<35
Trimetrevate
Severe>45
LACTATE DEHYDROGENASE
-USED AS A PROGNOSTIC MARKER
1-3 BETA D GLUCAN
-ELEVATED PLASMA LEVEL

low toxicity and greater efficacy

AHMAD
DANIEL
BIN ISM LIAW
AIL (221
APPROA 0461)
CH OF I
NV.

Reference:
https://medlineplus.gov/lab-tests/cd4-lymphocyte-count/
https://www.ucsfhealth.org/conditions/hiv/diagnosis
Low Haemoglobin level: Indicates mild Anaemia
Low Lymphocytes level : indicates high risk of
developing life threatening infections
2. Blood Urea Serum Electrolyte: Indicates
gradual hyponatremia that result in minimal
symptoms.
3. Arterial Blood Gases: Normal
4. Covid-19 RT-PCR: Negative indicates virus was not found in the sample
5. Chest x-ray: Pneumocystis carinii pneumonia is a fungal infection due to weaken
immune system or immunosuppression. (Opportunistic respiratory infection)
5. Sputum Examination:
Monoclonal immunofluorescent Ab for
pneumocystis Ag: positive indicates presence of
fungal infection (opportunistic infection)
Silver stains: Clusters of cysts pneumocystis carinii
were seen that indicate fungal infection
(opportunistic infection
6. Blood Culture & Sensitivity: Negative. No bacteria or
fungal were seen in the blood
7. Stool examination: Presence of Cryptosporidium parvum.
Cause severe, chronic and possibly fatal diarrhoea
8. High Vaginal Swab Culture & Sensitivity: Presence of Candida albicans
have a high capacity for virulence and can be associated with infectious
processes.
9 & 10. ELISA and Particle agglutination (PA) test: presence of HIV Ab indicates
infection by HIV/AIDS.
11. T lymphocyte enumeration: Low CD4 count
Weakened immune system with a high risk of
developing life-threatening infections
12. HIV RNA Quantification assay: High viral load
High number of viral particles in each milliliter of
blood indicate infection is progressing.
What is CD4 count &
HIV Viral Load?
CD4 count
The CD4 count will aid in determining
the level of immunosuppression and,
thus, the range of Opportunistic
Infections to which the patient is
susceptible.
HIV Viral Load
The most useful measure of
responsiveness to antiretroviral drugs
and in early treatment failure will rise
before the CD4 count begins to fall.
5
 ADLINA BINTI
MOHAMAD KAMAL
(2217658)
CRYPTOSPORIDIUM
PARVUM INFECTION

References:
Murray, P. R., Pfaller, M. A., & Rosenthal, K. S. (2021). Medical microbiology. Elsevier.
Cryptosporidiosis: Background, Etiology and Pathophysiology, Epidemiology. (2022). EMedicine.
https://emedicine.medscape.com/article/215490-overview?reg=1
‌Centers for disease control and prevention. (2019, February 22). Pathogen & Environment | Cryptosporidium |
Parasites | CDC. Www.cdc.gov. https://www.cdc.gov/parasites/crypto/pathogen.html
 CRYPTOSPORIDIUM PARVUM INFECTION/
CRYPTOSPORIDIOSIS
caused by the apicomplexan Mode of infection:
protozoan Cryptosporidium Zoonotic infection-spread from animal reservoirs to
30 different species , C. hominis and humans
C. parvum most infect human person-to-person spread by fecal-oral and oral-anal
resistant to the usual water- routes
purification procedures (chlorination Symptoms:
and ozone) enterocolitis
watery diarrhea without blood
Definitive host – man Stomach cramps or pain
Habitat – small intestine Nausea
Vomiting
Distribution - worldwide
Fever
Incubation period: 7 to 10 days Weight loss

At risk population: Veterinary personnel, animal handlers, children, homosexual men,

and immunocompromised individuals, day care (due to cross-contamination)
 Life Cycle
Cryptosporidium species do not multiply outside the host
1. ingestion of oocyst
2. excystation occurs (upper GI).
3. The sporozoites are released and invade epithelial cells (a) of the
gastrointestinal tract
4. parasites undergo asexual multiplication (schizogony or
merogony) (b,c,d) and then sexual multiplication (gametogony)
producing microgamonts (male) and macrogamonts (female) (e)
5. fertilization of the macrogamonts by the microgametes develop
that sporulate in the infected host.
6. Two different types of oocysts are produced
thick-walled - excreted from the host (f)
thin-walled - involved in autoinfection (g)
Laboratory diagnosis
Oocysts is concentrated with the modified zinc sulfate centrifugal flotation
technique or the Sheather sugar flotation procedure. Specimens may be stained
using the modified acid-fast method
direct immunofluorescence assay
PCR assays

Treatment, Prevention, and Control

Nitazoxanide (nonimmunocompromised individuals)
paromomycin and azithromycin (HIV-infected patients)
Spiramycin (control the diarrhea in early stages of AIDS)

improved personal hygiene and sanitation

 M UHAM
H A K IM M A D IZA T
I B IN A Z
(2 2 115 0 L AN
P R IN C IP 7)
LE OF M
N G.

dont forget to insert reference link

In the process of assessing the possibility of HIV infection, the following steps are
recommended.

1. Risk Assessment

2. Establish Diagnosis

3. Ascertain Stage

4. Useful laboratory tests

5. Initiate antiretroviral therapy

6. Initiate PCP prophylaxis

 Group 1 HIV disease
Asymptomatic Phase (Group 2)
(acute
seroconversion illness)
Acute seroconversion illness usually
presents as acute flu-like illness, or
mononucleosis-like illness which
presents 2-4 weeks after the initial HIV
infection. The symptoms include:
• fever
• arthralgia
• malaise
• myalgia
disease
The asymptomatic phase can last
for 3-7 years from the initial HIV
infection.
During this phase the patient feels
and looks well. Their CD4+ T-cell
counts can be normal.
It is recommended that these
individuals be counselled towards
change of behaviour, maintain
good health and practise behaviour
that will prevent further
transmission of HIV.
Symptomatic Phase
(Group 3 and Group 4) disease
It is difficult to predict how soon an HIV-infected
person will develop AIDS; however there are clinical
predictors that can be used as a guide:
• herpes zoster (multi-dermatornal)
• oral candidiasis
• oral hairy leukoplakia
• Prolonged fever, might sweets
• Progressive weight loss
Laboratory predictors of progression to AIDS:
• thrombocytopenia
• falling CD4+ T. cell counts
• high p24 antigen
HIV (Human Immunodeficiency Virus)
Treatment = Antiretroviral Therapy (ART)

1. Daily use of a combination of HIV medicines to treat HIV patients

2. ART does not cure HIV but it helps HIV patients to live longer and healthy
lives

Goal of ART are to:

reduce viral load to
undetectable level
improve CD4+ count
improve quality of life
reduce HIV
transmission
 Nucleoside reverse transcriptase inhibitors
(NRTIs) - block an enzyme called reverse
transcriptase
Non-nucleoside reverse transcriptase
inhibitors (NNRTIs) - bind to and later change
reverse
transcriptase
Integrase inhibitors, also called integrase
strand transfer inhibitors (INSTIs), - block an
enzyme called integrase
Protease inhibitors (PIs)- block an enzyme
called protease
Fusion inhibitors block - HIV from
entering the cells
CCR5 antagonists and post-attachment
inhibitors - block different molecules on
the CD4 cells. To infect a cell, HIV has to
bind to two types of molecules on the
cell's surface. Blocking either of these
molecules prevents HIV from entering
the cells.
Attachment inhibitors bind to a specific
protein on the outer surface of HIV. This
prevents HIV from entering the cell.
Diarrhoea (Cryptosporidium parvum)
Crofelemer for the relief of diarrhea in patients with HIV/AIDS who are
undergoing antiretroviral therapy

It blocks the chloride blocks chloride secretion and accompanying high-

volume water loss in diarrhea

If a particular antiretroviral medication is the culprit (eg, ritonavir), alternative

medications should be substituted, whenever possible
 Pneumonia (Pneumocystis carinii)
Pneumocystis carinii pneumonia (PCP) is a common opportunistic infection
occurring in HIV infected individuals.

In 80% of cases it is the first indicator of the development of AIDS.

Usually these patients will have a CD4+ T- lymphoeyte counts of less then 200/uL or a
CD4+/CD8+ ratio of less then 20%.

If the patient is not acutely ill, oral cotrimoxazole, 4 tablets 6 hourly for 14
days is adequate.

Intravenous or inhaled pentamidine isethionate can be used as a second line therapy

 SYARAH AISYA (2218886)

ISLAMIC PRACTICE IN
PREVENTION INFECTIOUS
DISEASE

Source:
Deuraseh , N. D. (2008). Protection against stds: An Islamic criminal law approach - JSTOR. Protection
against STDs: An Islamic Criminal Law Approach. Retrieved March 20, 2023, from
https://www.jstor.org/stable/27650610
Prohobition and punishment
of adultery
Those who fornicate - whether female or male - flog
each one of them with a hundred lashes.2 And let not
tenderness for them deter you from what pertains to
Allah's religion, if you do truly believe in Allah and the
Last Day3; and let a party of believers witness their
punishment
Engage in sexual contact only with one
partner who is having sex only with
you.
Both you and your partner should be
tested for HIV and other sexually
transmitted diseases.
Stay home if you are sick
The Prophet said:'Those with contagious disease
should be kept away from those who are
healthy"

Limit outdoort's important that if you're unwell you stay at

home to stop the spread of the infection to others.
Keep your distance (at least 1 metre away) from other
members of your household to stop them from getting ill
as well.
Immunise against infectious diseases:Vaccines
From Abu Hurairah RA, the Prophet PBUH
said:
‫َم ا َأْنَز َل ُهَّللا َد اًء ِإاَّل َأْنَز َل َلُه ِش َف اًء‬
Available vaccines for infetious disease
There is no disease that Allah has created,“ Cholera.
except that He also has created its
COVID-19 (corona virus)
”.treatment
Dengue.
Diphtheria.
Haemophilus influenzae type b
(Hib)
Human papillomavirus (HPV)
Influenza.
Practice good-food safety techniques
Precautions will help killing microbes present in the food :

Rinse all meat, poultry, fish, fruits, and vegetables under running water
before cooking or serving them

Separate raw foods and cooked foods. Don't use the same utensils or
cutting boards with cooked meat that were used to prepare the raw meat
without washing between uses.

Do not eat uncooked vegetables, including lettuce; do not eat fruit you
haven't peeled yourself

Avoid consuming ice while traveling. Freezing does not kill all water-borne
infectious microbes.
 Washing Hands Properly
Aisha reported :The Meaaenger of Allah if he
wanted to eat or drink ,he would first wash
his hands and then eat or drink'"