THIS IS AN ONLINE E LOG BOOK TO DISCUSS OUR PATIENT'S DE-IDENTIFIED HEALTH DATA SHARED AFTER TAKING HIS SIGNED INFORMED CONSENT. HERE WE DISCUSS OUR PATIENT'S PROBLEMS THROUGH SERIES OF INPUTS FROM AVAILABLE GLOBAL ONLINE COMMUNITY EXPERTS WITH AN AIM TO SOLVE THE PATIENT'S CLINICAL PROBLEMS WITH COLLECTIVE CURRENT BEST EVIDENCE BASED INPUTS.
[9.46 pm, 19/01/2026] PPM 1: EMR summary:
*Diagnosis*
DENGUE FEVER (NS1 POSITIVE STATUS IGM POSITIVE)
MALARIA
*Case History and Clinical Findings*
PATIENT C/O FEVER WITH CHILLS (HIGH GRADE) MORE DURING AFTERNOON SINCE 10 DAYS
C/O COUGH WITH SPUTUM SINCE 1 WEEK TO 10 DAYS
HISTORY OF PRESENTING ILLNESS: PATIENT WAS APPARENTLY ASYMPTOMATIC 7-10 DAYS AGO NOW CAME WITH THE COMPLAINTS OF FEVER WITH CHILLS HIGH GRADE MORE DURING AFTERNOON, INTERMITTENT RELIEVED ON MEDICATION A/W COLD, HEADACHE.
PT C/O COUGH WITH SPUTUM SINCE 7-10 DAYS WHICH IS SUDDEN IN ONSET GRADUALLY PROGRESSIVE A/W SPUTUM PRODUCTION WHITE IN COLOUR NON FOUL SMELLING NON BLOOD TINGED.
NO C/O SOB, ORTHOPNEA, PND, SWEATING, PALPITATIONS.
NO C/O ABDOMINAL PAIN, IRREGULAR BOWEL AND BLADDER HABITS. NO C/O LOSS OF APPETITE, LOC, GIDDINESS, INVOLUNTARY MOVEMENTS OF UL AND LL, DIFFICULTY IN SALLOWING, BLURRING OF VISION.
*Past History:*
N/K/C/O T2DM, HTN, TB, ASTHMA, COPD, CAD, EPILEPSY, THYROID DISORDERS.
*Personal History:*
- MARRIED, LABOURER, APPETITE NORMAL, MIXED DIET, REGULAR BLADDER HABITS, CONSTIPATION PRESENT, ADEQUATE SLEEP, NO ALLERGIES, OCCASIONAL ALCOHOL CONSUMPTION SINCE 15 YEARS.
*KIMS HOSPITALS
*GENERAL EXAMINATION:* MILD PALLOR, NO ICTERUS, NO CYANOSIS, NO CLUBBING, NO LYMPHADENOPATHY, NO PEDAL EDEMA.
*VITALS:* TEMP: 102 F, BP: 100/70MMHG, RR: 18 CPM, PR:94 BPM
*SYSTEMIC EXAMINATION*
CVS- S1 S2 PRESENT, RS-BAE +, NVBS, PER ABDOMEN- SOFT, OBESE
*CNS:*
POWER: RT - UL /5, LL /5; LT- UL /5, LL /5
TONE RT-UL -NORMAL, LL -NORMAL; LT- UL -NORMAL, LL -NORMAL
REFLEXES: RT: B +2, T +2, S +1, K +2, A +1, P FLEXOR
LT: B +2, T +2, S +1, K +2, A +1, P -FLEXOR
UROLOGY REFERRAL WAS DONE AND THEIR ADVICE WAS FOLLOWED.
*Investigation*
*HEMOGRAM (16/1/26):* HB-11.0, PCV-32.6 TLC-11 100, RBC-4.7, PLT- 26000
*HEMOGRAM (17/1/26):* HB-11.6, PCV-36.5 TLC-25.91, RBC-5.36, PLT- 28000
*HEMOGRAM (18/1/26):* HB-12.2, PCV-36.6 TLC-18 600, RBC-5.4, PLT- 70000
*HEMOGRAM (19/1/26):* HB-19.5, PCV-30.3 TLC-15000, RBC-4.4, PLT- 80000
*RFT(16/1/26):* UREA- 30 CREATININE-0.90, SODIUM-136, POTASSIUM-4.1, CHLORIDE-99
*SERUM ELECTROLYTES (17/01/26)* SODIUM-137, POTASSIUM-4.8, CHLORIDE-98 IONISED CALCIUM 1.10
*LFT(16/1/26):* TB 3.16 DB 0.89 SGPT 30 SGOT 51 ALP 214 TP 4.8 ALB -2.65 GLO-2.15 A/G 1.23
*LFT(19/1/26):* 1.52 DB 0.8 SGPT 25 SGOT 26 ALP 161 TP 5 ALB -2.5 GLO-2.5 A/G 1
*CUE (16/1/26):* PALE YELLOW CLEAR, ACIDIC, ALBUMIN NIL, URINE TO KETONE BODIES - NEGATIVE NIL PUS CELLS 2-3 EPITHELIAL CELLS 2-3, RBC-NIL, CASTS, CRYSTALS - NIL
*PT - 16.0 APTT-32.00 INR-1.11*
*TROP I - 9.50*
*SEROLOGY- NEGATIVE*
DENGUE IGM - POSITIVE
MALARIAL STRIP TEST - POSITIVE
*2D ECHO SCREENING WAS DONE AND IMPRESSION:* EF-62%
TRIVIAL TR+, NO PAH, NO MR/ PR/ AR
NO RWMA.NO AS/MS RVSP -32MMHG
GOOD LV SYSTOLIC FUNCTION
NO DIASTOLIC DYSFUNCTION.
IVC SIZE (0.9CMS) COLLAPSING
USG ABDOMEN AND PELVIS:
HEPATOMEGALY WITH GRADE I FATTY LIVER
SPLENOMEGALY
MILD HYDROURETERONEPHROSIS
MINIMAL FREE FLUID IN THE PELVIS
Treatment Given (Enter only Generic Name)
IV FLUIDS RL@ 100ML/HR
INJ NEOMOL 1GM IV/SOS IF TEMP>101F
INJ THIAMINE 200MG IV/BD 1-0-1
INJ ZOFER 4MG IV/SOS
INJ FALCIGO 120MG IV 1-0-1
TAB.PRIMAQUINE 15MG PO/OD 1-0-0
CAP DOXYCYCLINE 100MG PO/BD
SYP ASCORIL 15ML PO/TID 15ML-15ML-15ML
WATCH FOR ANY BLEEDING MANIFESTATION
BP MONITORING AND TEMPERATURE CHARTING 4TH HOURLY
Advice at Discharge
DRINK PLENTY OF ORAL FLUIDS
INJ.FALCIGO 120MG IV @10PM
TAB. THIAMINE 200MG PO/BD 1-0-1 X15DAYS
TAB.ZOFER 4MG PO/SOS
TAB.PRIMAQUINE 15MG PO/OD 1-0-0 X 14 DAYS
TAB.DOLO 650 MG PO/TID 1-1-1
19/01, 12:25]hu2: Currently admitted 25M patient with fever and thrombocytopenia since 7 days.
@ is it possible that the incidental finding of vivax parasites here is due to persistent hepatic phase while his current issues are due to dengue?
[19/01, 13:00]hu1: In clinical practice, seeing Plasmodium vivax on a peripheral smear in a patient with fever and thrombocytopenia is rarely "incidental," even if a co-infection like Dengue is suspected.
Here is a breakdown of why the parasites you see are likely active and how to approach this:
1. Erythrocytic Phase vs. Hepatic Phase
Technically, if you can see the parasites on a blood smear, they are in the erythrocytic (blood) phase, not the hepatic phase.
* Hepatic Phase (Hypnozoites): These are dormant in the liver and are completely invisible on a peripheral blood smear.
* Erythrocytic Phase: Once the parasites emerge from the liver and enter the bloodstream, they begin invading red blood cells. This is the stage that causes fever and thrombocytopenia.
2. The Possibility of Co-infection
It is quite common in endemic regions for patients to have Dengue and Malaria co-infection.
* Overlapping Symptoms: Both Dengue and Malaria cause high fever, severe headache, myalgia, and thrombocytopenia.
* Incidental finding? While "asymptomatic parasitemia" (carrying malaria without symptoms) exists in high-transmission areas, if a patient is symptomatic (fever/low platelets), the malaria parasites are usually considered a primary cause of the illness until proven otherwise.
3. Comparing the Two
| Feature | Plasmodium vivax | Dengue Virus |
|---|---|---|
| Thrombocytopenia | Very common; often due to splenic sequestration or immune destruction. | Hallmark; due to bone marrow suppression and platelet consumption. |
| WBC Count | Often low (leukopenia). | Often low (leukopenia). |
| Smear Finding | Visible parasites (Trophozoites/Gametocytes). | No visible organisms; may see atypical lymphocytes. |
| Timeline | Can be acute or a relapse (weeks/months later). | Acute (usually 3–10 days). |
Clinical Recommendation
If you suspect Dengue is the "true" driver of the current symptoms, you should confirm it with:
* Dengue NS1 Antigen: Most sensitive in the first 5 days.
* Dengue IgM/IgG: Useful after day 5–7.
* Hematocrit (Hct) Monitoring: A rising hematocrit alongside falling platelets is a strong indicator of Dengue (capillary leak), whereas Malaria usually causes a stable or falling hematocrit (due to hemolysis).
Note: Even if the Dengue test is positive, the Malaria must be treated. A "minor" malaria infection can quickly become severe if ignored, and the combination of both infections significantly increases the risk of severe thrombocytopenia and organ dysfunction.
Would you like me to help you interpret any specific lab values for this patient, such as their Hematocrit or White Cell count?
[19/01, 13:10]hu3: Sir, the hepatic phase of Plasmodium vivax (hypnozoites) is clinically silent and does not produce parasitemia. So, if vivax parasites are seen on the peripheral smear, it indicates an active blood-stage infection either a relapse or an ongoing infection.
The thrombocytopenia and fever could be due to vivax itself or due to a possible co-infection like dengue, I think they should be further test to rule like HCT and dengue igM and igG
[19/01, 14:39]hu2: Very interesting counterpoints 👏👏
So let's look at what are the possibility of this being an active vivax infection with thrombocytopenia. @Meta AI @Dr. I'm sure there are papers and reports that can demonstrate that it's epidemiologically documented but then I would expect that with severe vivax and here as per @Pushed1Comm22 @Anonymous Pm the patient appears to be recovering.
[19/01, 14:39] Meta AI: Sounds like you're digging deep into the clinical presentation of Plasmodium vivax malaria 😊.
You're spot on that the presence of vivax parasites on the peripheral smear indicates an active blood-stage infection, which could be either a relapse or an ongoing infection. Given the thrombocytopenia and fever, it's reasonable to consider co-infections like dengue, especially in endemic areas.
To further evaluate this, I'd suggest looking into the patient's:
- Travel history
- Previous malaria episodes
- Response to antimalarial treatment
- Platelet count trend
Thrombocytopenia is common in vivax malaria, but severe thrombocytopenia might warrant investigation for co-infections or other causes.
Want to explore the treatment approach for this patient or discuss the likelihood of co-infection?
[19/01, 14:42]hu2: More inputs from Microbiology expert s:
[19/01, 14:09] Microbology:
Ring forms within the RBC
[19/01, 14:12] Microbology:
It is looking like vivax trophozoites.
Single ring form in RBC
[19/01, 14:18] generalist:
Thanks.
Can these even be incidental to the current patient who has more features of dengue than vivax?
Perhaps he had an acute vivax earlier and currently these are just the left over spillovers from the hepatic phase of his earlier vivax?
[19/01, 14:21] Microbology:
But many ring forms are seen in this field.
If periodic typical episodic type of fever is not present, then it
may be atypical symptomatology
[19/01, 14:25] Microbology:
Even if it is relapse due to hypnozoites (dormant forms from hepatocytes), it is significant infection as multiplication) is taking place.
[19/01, 14:59]hu2: Another input in pm:
A total of 131 patients were included in the study with a diagnosis of malaria. We excluded 11 of the screened patients by the exclusion criteria. The majority of study participants 112 (86%) were male. None of the study patients were pregnant. The mean age of the patients was 39 years. Sixty-two per cent of the patients were in the age group of 20–40 years. Sixty patients (46%) were infected with P. vivax, while 46 (35%) had non-severe and 24 (18%) had severe falciparum infection who met the WHO 2000 severity criteria at any time during hospitalization. There was one (1%) case of mixed infection with both P. vivax and P. falciparum; none of the P. vivax cases had complicated malaria. The mean platelet count in patients with vivax malaria was 94×109/l±48, in patients with uncomplicated falciparum malaria, 100×109/l±64, and in patients with complicated malaria, 43×109/l±24 (Fig. 1 and Table 1). The platelet count in the patient with mixed infection was 18 000×109/l. There was no significant statistical difference in mean platelet count between the patients with vivax malaria and non-severe falciparum malaria. Compared to non-severe falciparum malaria, severe falciparum malaria was associated with a significantly lower mean platelet count (43×109/l versus 101×109/l; P = 0.01). There was an inverse relationship between the percentage of infected erythrocytes in falciparum malaria and platelet count (P = 0.03) (Fig. 2).
Platelet count in vivax and falciparum malaria.
[19/01, 15:18]hu1: It is an insightful clinical question. While your hypothesis about Dengue being the primary driver is plausible, the biological reality of malaria makes the "incidental" finding of parasites on a smear quite significant.
1. The "Incidental" Paradox: Blood vs. Liver
The most important biological distinction is that if you see parasites on a peripheral smear, the infection is in the Erythrocytic (Blood) Phase.
* The Hepatic Phase (Hypnozoites): These are dormant in the liver and are completely invisible on blood smears. They do not cause thrombocytopenia or fever while in the liver.
* The Blood Phase: For a parasite to be visible in a Red Blood Cell (RBC), it has already emerged from the liver and is actively replicating in the blood.
Therefore, seeing P. vivax is not just an "incidental" marker of a past infection; it indicates an active, current blood-stage infection.
2. Can P. vivax cause severe thrombocytopenia?
Historically, P. vivax was called "benign tertian malaria," but modern evidence has debunked this.
* Epidemiological Evidence: Large meta-analyses (e.g., Naing et al., 2014) have shown that P. vivax can cause severe thrombocytopenia (<50,000/\mu L) at rates comparable to P. falciparum.
* Mechanism: It’s not just about parasite density. P. vivax triggers an intense systemic inflammatory response (cytokine storm) that leads to peripheral platelet destruction and splenic sequestration.
3. The "Recovery" Scenario
If the patient appears to be recovering despite the presence of parasites, there are three likely explanations:
* Dengue-Dominant Co-infection: You might be correct that Dengue was the "louder" infection. If the patient is on day 7, they may have just passed the "Critical Phase" of Dengue (days 3–6) and are now entering the Recovery Phase, where fluid is reabsorbed and platelets begin to rise spontaneously.
* Partial Immunity: In endemic regions, patients often have "clinical immunity." They may harbor low-level parasitemia that their immune system "contains," preventing it from becoming a fulminant, life-threatening malaria case even without immediate treatment.
* Recent Treatment: If the patient was started on any antimalarials (even a single dose of Artemisinin-based Combination Therapy or Chloroquine), the clinical symptoms often improve within 24–48 hours, even if a few residual parasites are still visible on the smear for another day or two.
4. Why you must treat the "Incidental" Vivax
Even if Dengue caused the initial crisis, the P. vivax cannot be ignored for two reasons:
* The "Double Hit": The patient’s marrow is already stressed by Dengue. If the P. vivax bloom continues, it can cause a second, deeper drop in platelets or trigger severe anemia.
* The Relapse: Without treating the liver phase (using Primaquine or Tafenoquine), the patient will almost certainly experience a relapse in the coming weeks or months once the "dormant" hypnozoites wake up.
Summary Table: Dengue vs. Vivax in the Recovery Phase
| Feature | Dengue (Day 7-10) | P. vivax (Untreated) |
|---|---|---|
| Platelet Trend | Usually rising (Recovery phase) | Usually falling or low |
| Hematocrit | Normalizing (after previous rise) | Slowly falling (Hemolysis) |
| Clinical State | Improving appetite, "Dengue rash" | Recurring fever spikes (Tertian pattern) |
Next Step: Would you like to check the patient's Hematocrit or Mean Platelet Volume (MPV)? A high MPV often suggests that the bone marrow is actively pushing out new, young platelets, which is a good sign of recovery.
[19/01, 16:35]hu2: Thanks
Here's the patient's serial platelet counts attached
He was dengue ig M positive and ns1 negative.
I agree with the notion of partial immunity with a contained infection albeit visible in the blood which matches with the notion of disease activity not necessarily depending on organism activity but more spiked by the host's immune system activity to the antigen. Similarly how people are infected with TB and are mantoux positive and yet not diseased,. similar to the spectrum of COVID positive people who can range from being asymptomatic to being on the ventilator!
[8:10 am, 20/01/2026] Rakesh Biswas Sir: This is a sophisticated clinical observation. Your hypothesis that the Plasmodium vivax parasitemia could be a "bystander" while Dengue is the primary driver is strongly supported by the patient's laboratory trends and known immunological mechanisms in endemic regions.
1. Evidence from the Platelet Trend
The serial platelet counts you provided (extracted below) tell a classic story of Dengue recovery:
| Date/Time | Platelet Count (\times 10^3/\mu L) | Phase |
|---|---|---|
| 14/10/24 23:36 | 134 | Early Acute |
| 16/10/24 07:05 | 73 | Critical Phase |
| 17/10/24 13:58 | 44 (Nadir) | End of Critical Phase |
| 18/10/24 14:38 | 61 | Recovery Phase Begins |
| 19/10/24 14:15 | 83 | Active Recovery |
The patient is currently on Day 7 of illness. The transition from a nadir of 44 to a rise of 83 within 48 hours—coupled with Dengue IgM positivity and NS1 negativity—is the "smoking gun" for the Dengue recovery phase. NS1 typically disappears after day 5, while IgM peaks around day 7.
2. The "Incidental" Parasitemia: "Premonition" and Immunity
Your analogy to Mantoux-positive TB or asymptomatic COVID is excellent and corresponds to a well-documented phenomenon in malariology called "Premonition" (or Clinical Immunity).
* Asymptomatic Parasitemia: In highly endemic areas, up to 10–20% of the "healthy" population may have visible P. vivax on a smear without fever or thrombocytopenia. Their immune systems have learned to tolerate the parasite's presence, keeping the inflammatory cytokine response (TNF-\alpha, IL-6) below the "pyrogenic threshold."
* The "Double Hit": It is entirely possible that this patient was an asymptomatic carrier of P. vivax when they contracted Dengue. The Dengue virus then caused the clinical "disease" (the 7-day fever and the drop to 44k platelets), while the P. vivax remained a passive traveler.
3. A Third Possibility: The "Trigger" Effect
There is another fascinating clinical layer: Did the Dengue trigger the Malaria? Recent literature suggests that the systemic inflammation and "cytokine storm" caused by a primary infection (like Dengue or even COVID-19) can actually reactivate dormant hypnozoites in the liver.
* Essentially, the "stress" of the Dengue infection may have "woken up" the liver-stage vivax, pushing it into the blood.
* Even if this happened, if the patient has partial immunity, they might not show the classic "malarial paroxysms" (shivering/rigors), making the finding look incidental while they recover from the Dengue.
Clinical Interpretation
You are likely correct that Dengue is the primary actor here, specifically because the platelet recovery is following the standard 7-day viral arc.
However, the "Incidental" Vivax is still clinically dangerous:
* Risk of Post-Dengue Slump: As the patient's immune system is exhausted by Dengue, the P. vivax could "bloom" and cause a secondary drop in platelets or a new fever spike in a few days.
* The Carrier State: To ensure the patient doesn't have a true malarial relapse in 2 months, the liver stage (hypnozoites) must be cleared.
Recommendation: Treat the P. vivax as per protocol (e.g., Chloroquine + Primaquine/Tafenoquine) even if the patient looks better today. The rise in platelets from 44 to 83 is a "Dengue Win," but the visible parasites are a "Malaria Warning."
Would you like to see the specific papers discussing how Dengue triggers Malaria relapses?
[8:10 am, 20/01/2026] PPM 1: Thanks.
Yes those specific papers would be a useful read
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