FEVER AND

PALLOR
ADZU SOM LEVEL 1
Group 6
Adjarani, Antoque, Calo, Francisco, Gaganting,
Isnang, Karay, Pingay, Sakirani, Tocao
critiQUE
of initial
treatment
PRE-ADMISSION MANAGEMENT

CHLORAMPHENICOL suspected
was prescribed to the patient typhoid
by a private practice physician fever?

Phenicols | Broad-spectrum Bacteriostatic Antibiotic

Has effect of typhoid fever, but no effect on Plasmodium spp.
In the case of malaria-induced hemolysis, it can be mistaken for
iron-deficiency anemia hence the iron supplementation given
 suspected
PRE-ADMISSION MANAGEMENT typhoid fever?

Should Have Been: before prescribing

Malaria Rapid Diagnostic Test (RDT) – CHLORAMPHENICOL
Quick bedside test for Plasmodium
antigens. has adverse
Peripheral Blood Smear (Thick and
effects!
Thin Smear) – Gold standard to confirm
Plasmodium species and parasitemia
level.
benefits should
Typhoid Tests (e.g., blood culture for
Salmonella Typhi, Widal test if outweigh risk
available but less reliable).
post-ADMISSION MANAGEMENT

whole blood
transfusion FOR MALARIAL
150 cc of Fresh Whole ANEMIA
Blood (Patient is a type B)

Severe malarial anemia 📕 Nelson’s Textbook in Pediatrics, 22nd ed. (2024)

Defined as the presence of P. falciparum parasitemia in an individual with a
hemoglobin of <5 g/dL. In endemic areas, WHO includes a parasitemia cutoff of
>10,000 parasites per microliter for this definition.
post-ADMISSION MANAGEMENT

Should Have Been:

The patient had Hb 4.5 g/dL and
tachycardia (HR = 144 bpm), which
justified transfusion.
Whole blood transfusion increases the risk of
volume overload and hyperkalemia in young
children. Thus, Packed RBCs are prefered
WB Transfusion increases the
The patient could also receive iron and folate risk of volume overload
to support RBC production after transfusion.
unless active bleeding is present
 post-ADMISSION MANAGEMENT

FOR SEVERE MALNUTRITION

If very severe anemia (or Hgb 4-

6 g/dL and respiratory distress):

Give whole blood 10 mL/kg

slowly over 3 hr.
(120 cc for our patient)
If signs of heart failure, give
5-7 mL/kg packed cells
rather than whole blood
(min: 60 cc for our patient)
Nelson’s Textbook on Pediatrics (22nd edition), page 428
ruling-in
malaria
presentation of differentials
 Rule in Rule OUT

References:
Nelson, Pediatric Symptom-Based Diagnosis, 2nd Edition
Nelson, Textbook of Pediatrics, 20th Edition
Robbins and Kumar, Basic Pathology 11th Edition
 Rule in Rule OUT

References:
Nelson, Textbook of Pediatrics, 20th Edition
malaria
epidemiology, pathogenesis
and complications
 malaria
Leading parasitic disease that cause mortality.
Transmission: through bite of an infected female Anopheles mosquito

Plasmodium Species involved:

Plasmodium falciparum
Plasmodium vivax
Plasmodium ovale
Plasmodium malariae
Plasmodium knowlesi

Reference:
Belizario, Jr, V. Y., & De Leon, W. (2013). Medical Parasitology in the Philippines. The University Of The Philippines Press.
Kumar, V., Abbas, A. K., & Aster, J. C. (2018). Robbins Basic Pathology (10th ed.). Philadelphia, Pennsylvania Elsevier.
Riedel, S., Morse, S. A., Mietzner, T., & Miller, S. (2019). Jawetz Melnick & Adelbergs Medical Microbiology (28th ed.). McGraw Hill Professional.
 1. Cold Stage
2. Hot/Febrile Stage
malaria 3. Sweating Stage

Incubation Parasitized Level of Fever

Species Term
Period Red Cells Parasetemia Paroxysms

> 200,000/ μL;

P. falciparum 8-15 days All ages Common 50,000/μL
48 hrs Tertian Fever

P. vivax 12-20 days Young RBC Up to 30,000/ μL 48 hrs Tertian Fever

P. ovale 11-16 days Young RBC < 10,000/μL 48 hrs Tertian Fever

P. malariae 18-40 days Aging Cells < 10,000/μL 72 hrs Quartan Fever

P. knowlesi Not stated All ages Not stated 24 hrs Quotidian Fever

Reference:
Belizario, Jr, V. Y., & De Leon, W. (2013). Medical Parasitology in the Philippines. The University Of The Philippines Press.
Kumar, V., Abbas, A. K., & Aster, J. C. (2018). Robbins Basic Pathology (10th ed.). Philadelphia, Pennsylvania Elsevier.
Riedel, S., Morse, S. A., Mietzner, T., & Miller, S. (2019). Jawetz Melnick & Adelbergs Medical Microbiology (28th ed.). McGraw Hill Professional.
 Most Common Species
P. vivax
P. falciparum (deadliest)
epidemiology
Endemicity
Hypoendemic (<10%)
Mesoendemic (11-50%)
Hyperendemic (51-75%)
Holoendemic (>75%)

Source: Lange, Jawetz, Melnick, and Adelbergz Medical Biology 28th Ed., 2019 and
Harrison’s Principle of Internal Medicine 21st Ed., 2022
 Incidence Rate
Worldwide
Estimated 263 million cases and 597 000
malaria deaths worldwide in 2023
Philippines
epidemiology 6,248 cases were recorded in 2023, with
a +90% increase in estimated cases from
2022-2023.
Of the 82 provinces, Palawan remains the
only province with active cases. It
reported a total of 6,188 malaria cases in
2023.

Source: World Health Organization, 2024

 Groups at Risk
Children under 5
Pregnant women and girls
Travelers
epidemiology
People with HIV/AIDS
People with disabilities, and
People in remote areas with limited healthcare
access

Source: DOH Research Institute for Tropical Medicine, 2024

LIFE CYCLE
WHO
CRITERIA
ON SEVERE
MALARIA

Reference: Kliegman, R., & St. Geme, J. W. (Eds.). (2024). Nelson textbook of pediatrics (22nd ed.). Elsevier. Â
 P. falciparum
60% parasitemia (>500,000/uL)
infects both immature and mature erythrocytes

P. vivax
severe anemia
splenic rupture

causative P. ovale
least common
respiratory symptoms resolve with medication
agents P. malariae
mildest
most chronic but unmasked when ->
immunosuppression; physiologic stress
Nephrotic syndrome

P. knowlesi
uncomplicated
can lead severe malaria
 P. falciparum
increased parasitemia
Severe increased proinflammatory cytokines
cytoadherence at vascular endothelium
malaria polyclonal activation
paradite aerobic metabolism

Reference: Kliegman, R., & St. Geme, J. W. (Eds.). (2024). Nelson textbook of pediatrics (22nd ed.). Elsevier. Â
Complica
-tions

Reference: Kliegman, R., & St. Geme, J. W. (Eds.). (2024). Nelson textbook of pediatrics (22nd ed.). Elsevier. Â
paraclinicals
expected results
overview of malarial smear
detection of plasmodium parasites
overview of malarial smear
detection of plasmodium parasites

Ask for MP test in all cases of fever and related

symptoms and also whenever there is high level of
suspicion

MP test can be done at any time. Do not wait for

typical symptoms and signs or for chills

A negative test DOES NOT rule out malaria.

Repeated tests may have to be done in all doubtful
cases. Duration of the illness, level of parasitemia,
expertise of the technician and the method of
examination may all have a bearing on the result of
the M.P. test
 stages of plasmodium in the
blood and their smear findings
Malaria parasites undergo asexual replication inside RBCs (erythrocytic stage).
The smear detects forms of Plasmodium during this stage.
 methods for
computing parasitemia
expected findings Patient findings
Normal
Result
Range

Hematocrit 7 (low) 11.5 - 14.5

4,000 -
WBC 12,000
12,000

Neutrophils 24% (high) 54 - 62%

Lymphocytes 76% (high) 25 - 35%

expected findings Patient findings
Normal
Result
Range

Hematocrit 7 (low) 11.5 - 14.5

4,000 -
WBC 12,000
12,000

Neutrophils 24% (high) 54 - 62%

Lymphocytes 76% (high) 25 - 35%

treatment and
management
Life cycle of the malarial parasite, Plasmodium falciparum, showing the sites of action of antimalarial drugs
recap & case
presentation
CASE 2 We have a case of N.A., a 25-year-old housewife from
Basilan, who was admitted to ZCMC due to a chief
complaint of dizziness. The symptom started 6 days
PTA, described as a sudden onset of dizziness
associated with fever and chills. There was no initial
consult or medications taken.

1 day PTA, the patient sought consultation with a

private physician, where she was prescribed an
antibiotic and an antipyretic, which provided temporary
relief. However, due to persistence of symptoms, the
patient was brought to ZCMC for further evaluation
and was subsequently admitted.
CASE 2 Chief Complaint: sum
DIZZINESS
ma
ry

History of Present Illness:

Onset: 6 days PTA
Assoc. s/sx: Fever and Chills

Past Medical History:

Unremarkable
case 2
physical exam Vital Signs:
Conscious, weak

T - 39.7ºC
PR - 112 BPM
RR - 20 cpm
BP - 110/60 mmHg
case 2 HEENT:
physical exam
(+) Slight icteric sclerae
(+) Pale palpebral conjunctivae
Chest:
Symmetric chest expansion
Lungs: (-) Rales
Heart: (-) Murmur
Abdomen:
(+) Hepatosplenomegaly
case 2
paraclinicals Complete Blood Count:
Hematocrit = 0.22
White Blood Cells = 9.6
Segmenters = 0.44
Lymphocytes = 0.56

Malarial Smear:
(+) Plasmodium vivax III
case 2 Urinalysis:
paraclinicals Yellow, slighly cloudy

Pus cells = 0-33

RBCs = 0-1
Epithelial cells = +2
Bacterial cells = +2
Fine granular cast = 2-3
Course granular cast = 0-2
Amorphous urates = +4
clinical correlation
Malarial Smear
(+) P. vivax, primary diagnosis

Complete Blood Count

Anemia (Hct - 0.22) - Possibly due to
hemolysis of P. vivax
Lymphocytosis (56%) - mildly elevated
possibly due to parasitic infection (Malaria)
clinical correlation
Urinalysis
Slightly cloudy possibly reflecting renal response to
hemolysis, including presence of casts, urates, and
possibly proteins
Amorphous urates: increased uric acid due to
RBC breakdown, fever, dehydration
Fine casts: mild acute kidney involvement
Course casts: low count suggests low tubular
involvement
No active UTI (Pus cells: 0-3) | but (+) bacteria - possible
contamination
clinical correlation
1. Malarial Anemia
2. Possible malaria-associated AKI
treatment and
management
FEVER AND
PALLOR
ADZU SOM LEVEL 1
Group 6
Adjarani, Antoque, Calo, Francisco, Gaganting,
Isnang, Karay, Pingay, Sakirani, Tocao
 thank
you!
ADZU SOM LEVEL 1
Group 6
Adjarani, Antoque, Calo, Francisco, Gaganting,
Isnang, Karay, Pingay, Sakirani, Tocao
extra slides
 ribosomal protein
synthesis inhibitors
 30S RIBOSOMAL SUBUNIT
INHIBITORS
Aminoglycosides (e.g., gentamicin, streptomycin, amikacin)
Bind irreversibly to the 30S subunit → cause misreading of
mRNA → produce faulty proteins → bactericidal.
Require oxygen for uptake (ineffective against anaerobes).

Tetracyclines (e.g., doxycycline, minocycline, tigecycline)

Bind reversibly to the 30S subunit → block aminoacyl-tRNA
binding to the A-site → inhibit elongation → bacteriostatic.
 50S RIBOSOMAL SUBUNIT
INHIBITORS
Macrolides (e.g., erythromycin, azithromycin, clarithromycin)
Bind to the 50S subunit at the 23S rRNA → inhibit translocation
of peptidyl-tRNA from A-site to P-site → bacteriostatic.

Lincosamides (e.g., clindamycin)

Bind to the 50S subunit at the same site as macrolides → block
peptide bond formation → inhibit elongation → bacteriostatic.
 50S RIBOSOMAL SUBUNIT
INHIBITORS
Chloramphenicol
Binds to the 23S rRNA of the 50S subunit → inhibits peptidyl
transferase → prevents peptide bond formation → bacteriostatic.
Can cause aplastic anemia (rare but serious side effect).
Oxazolidinones (e.g., linezolid, tedizolid)
Bind to the 50S subunit → prevent the formation of the initiation
complex (fMet-tRNA binding) → bacteriostatic.
 50S RIBOSOMAL SUBUNIT
INHIBITORS
Streptogramins (e.g., quinupristin-dalfopristin)
Dalfopristin: Binds to 50S → enhances binding of quinupristin.
Quinupristin: Inhibits translocation → synergistic bactericidal effect.

MNEMONIC:
"Buy AT 30, CCEL at 50"
Aminoglycosides & Tetracyclines → 30S
Chloramphenicol, Clindamycin, Erythromycin
(Macrolides), Linezolid → 50S