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Case Analysis: 35-Year-Old Male with Fever, Convulsions & Altered Sensorium
Question 1: Provisional Diagnosis
Cerebral Malaria due to Plasmodium falciparum
Clinical clues:
- High-grade fever + altered sensorium (cerebral involvement)
- Convulsions
- Tachycardia (HR 105 bpm), tachypnea (RR 28 bpm), hypotension (BP 90/70)
- Low SpO2 (92%) - suggesting pulmonary involvement
CBC findings analysis:
| Parameter | Patient Value | Interpretation |
|---|---|---|
| Hemoglobin | 13.5 g% | Low-normal (mild anemia) |
| RBC | 4.05 million/µL | Slightly low |
| Hematocrit | 44.2% | Normal |
| MCV | 83.2 fl | Normocytic |
| MCH | 28.4 pg | Normal |
| MCHC | 32.6 g/dl | Slightly low |
| RDW-CV | 12.4% | Normal |
| WBC | 24.5 × 10³/µL | Leukocytosis |
| Neutrophils | 85% | Neutrophilia - acute infection |
| Lymphocytes | 11% | Relatively low |
| Monocytes | 2% | Normal |
| Eosinophils | 2% | Normal |
| Basophils | 0% | Normal |
| Platelets | 412 × 10³/µL | Normal |
Peripheral blood smear (from image): Shows RBCs with multiple intraerythrocytic ring forms - classic for P. falciparum. Multiple rings per cell, small delicate ring forms, and the presence of cells appearing to have parasitic inclusions are hallmark features.
The combination of:
- Fever + convulsions + coma = cerebral malaria
- Normocytic anemia = hemolytic destruction of RBCs
- High neutrophilic leukocytosis = active infection response
- Peripheral smear with ring forms = intraerythrocytic parasites
All point to P. falciparum malaria with cerebral involvement (Cerebral Malaria).
"Falciparum malaria, which has a unique morphology easily identifiable on the peripheral blood smear, is the predominant species of malaria that causes coma and death." - Rosen's Emergency Medicine
Question 2: Various Causes of Cerebral Malaria / Malaria with Neurological Manifestations
The pathophysiology behind cerebral malaria involves several mechanisms:
1. Cytoadherence & Microvascular Occlusion
P. falciparum-infected RBCs express PfEMP1 (Plasmodium falciparum erythrocyte membrane protein 1) on the cell surface, which binds to endothelial adhesion molecules (ICAM-1, VCAM-1, CD36). This causes parasitized RBCs to adhere to and obstruct cerebral capillaries - leading to ischemia, hypoxia, seizures, and coma. (Robbins Basic Pathology)
2. Rosetting
Parasitized RBCs bind to uninfected RBCs forming "rosettes," worsening microvessel obstruction and reducing cerebral perfusion.
3. Sequestration
Mature parasitized RBCs are sequestered in deep capillary beds (not visible on peripheral smear), leading to severe end-organ damage despite apparently low parasitemia.
4. Cytokine Storm / Inflammatory Response
Rupture of schizonts releases malarial antigens (including hemozoin - malarial pigment) which stimulate macrophages to release TNF-alpha, IL-1, IL-6. This causes:
- Blood-brain barrier disruption
- Cerebral edema
- Hyperpyrexia
- Altered consciousness
5. Hypoglycemia
P. falciparum rapidly consumes glucose + quinine (used in treatment) stimulates insulin release, causing severe hypoglycemia, which worsens neurological manifestations.
6. Anemia & Hypoxia
Destruction of RBCs causes hemolytic anemia, reducing oxygen-carrying capacity and worsening cerebral hypoxia - contributing to encephalopathy.
7. Nitric Oxide Depletion
Hemolysis releases free hemoglobin which scavenges NO. NO is needed for vasodilation; its depletion leads to endothelial dysfunction and vasoconstriction in cerebral vessels.
8. Metabolic Acidosis
Lactic acidosis from poor tissue perfusion (due to microvascular obstruction and anemia) contributes to cerebral dysfunction.
Key Teaching Point: The peripheral smear in P. falciparum characteristically shows:
- Multiple ring forms per RBC (double infection)
- Small, delicate rings with double chromatin dots ("applique/accolé" forms)
- Banana-shaped gametocytes (pathognomonic, seen in later stages)
- Absence of mature trophozoites/schizonts in peripheral blood (they are sequestered)
(Robbins & Kumar Basic Pathology; Rosen's Emergency Medicine; Fishman's Pulmonary Diseases)
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Histopathology: Acute Appendicitis
Question 1: Identification of the Lesion
Acute Appendicitis (Acute Suppurative Appendicitis)
The two H&E-stained sections show a cross-section of the vermiform appendix with hallmark features of acute inflammation. Key identifiers:
- Tubular organ architecture with mucosa, submucosa, muscularis propria, and serosa
- Large submucosal lymphoid follicle with germinal center (dark purple nodule visible in top image - characteristic of the appendix)
- Mucosal ulceration and transmural neutrophilic infiltrate
- Fibrinopurulent luminal exudate
Question 2: Two Microscopic Features
Feature 1: Neutrophilic Infiltration of the Muscularis Propria
- This is the diagnostic hallmark of acute appendicitis
- Polymorphonuclear neutrophils (PMNs) are seen infiltrating the muscular wall of the appendix
- In early appendicitis, there is a modest perivascular neutrophilic infiltrate within all layers; as it progresses, the infiltrate becomes dense and transmural
- Crypt abscesses (neutrophils within mucosal glands) and focal superficial mucosal ulceration are also present
"Diagnosis of acute appendicitis requires neutrophilic infiltration of the muscularis propria." - Robbins & Kumar Basic Pathology
Feature 2: Mucosal Ulceration with Fibrinopurulent Exudate
- Focal erosion and ulceration of the mucosal lining - normal surface epithelium is disrupted
- The lumen contains a fibrinopurulent exudate (mixture of fibrin strands, necrotic debris, and degenerated neutrophils)
- Submucosal edema and vascular congestion (dilated, blood-filled vessels) are seen separating connective tissue fibers
- The serosa becomes dull and granular (instead of its normal glistening appearance) due to serosal neutrophilic infiltration
Additional Microscopic Features Visible
| Feature | Significance |
|---|---|
| Prominent submucosal lymphoid follicle with germinal center | Normal appendiceal architecture |
| Transmural neutrophilic infiltrate | Indicates progression beyond early appendicitis |
| Stromal edema in submucosa | Vascular permeability from inflammation |
| Distorted crypts | Reactive change from acute inflammation |
| Congested subserosal vessels | Early vascular response |
Pathogenesis (Brief)
Obstruction (usually by a fecalith in 50-80% of cases) → raised intraluminal pressure → venous outflow compromise → ischemia + bacterial stasis → neutrophilic infiltration → if untreated: suppurative appendicitis → gangrenous appendicitis → rupture + peritonitis
(Robbins & Kumar Basic Pathology; Bailey and Love's Surgery)
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Case Analysis: 32-Year-Old Male, 7-Year Primary Infertility - Semen Analysis
Question 1: Diagnosis
Oligoasthenoteratozoospermia (OAT Syndrome)
Step-by-step analysis of the semen report against WHO normal reference values:
| Parameter | Patient Value | Normal Range | Interpretation |
|---|---|---|---|
| Volume | 2 ml | 2-6 ml | Normal |
| Liquefaction time | 40 min | 15-60 min | Normal (borderline) |
| Appearance | Grey | Viscous, White or Grey | Normal |
| pH | Alkaline | 7.2-8 | Normal |
| Sperm count | 3 million | ≥20 million/ml | SEVERELY LOW - Oligospermia |
| Sperm motility | 40% active, 60% non-motile | >50% motile | ABNORMAL - Asthenospermia |
| Sperm viability | 40% normal | >75% | LOW |
| Sperm morphology | 40% normal | >30% normal | Borderline acceptable |
| Agglutination | 40% normal | >30% | Borderline |
| Fructose test | Positive | Positive | Normal (seminal vesicle function intact) |
| Acid phosphatase | Nil | 1×10⁶/ml or <5/HPF | Normal |
| Leucocytes | Nil | Nil | No infection |
| RBC | Nil | Nil | Normal |
Summary of Defects:
- Oligospermia - sperm count 3 million vs normal ≥20 million (severely reduced, ~85% below normal)
- Asthenospermia - only 40% active motility vs required >50%; 60% non-motile
- Hypospermia of viability - 40% viable vs required >75%
Final Diagnosis: Oligoasthenospermia (Male factor primary infertility)
(Tietz Textbook of Laboratory Medicine; Smith and Tanagho's General Urology)
Question 2: Causes of Male Infertility
Causes are best classified as Pretesticular, Testicular, and Posttesticular:
A. Pretesticular Causes (Hormonal/Endocrine)
| Category | Examples |
|---|---|
| Hypothalamic disease | Kallmann syndrome (GnRH deficiency + anosmia), isolated FSH/LH deficiency |
| Pituitary disease | Hyperprolactinemia, pituitary tumors/infiltration, post-radiation damage |
| Exogenous hormones | Anabolic steroids, estrogen/androgen excess, glucocorticoid excess, hypothyroidism/hyperthyroidism |
| Growth hormone deficiency | Rare cause of impaired spermatogenesis |
B. Testicular Causes (Primary)
| Category | Examples |
|---|---|
| Chromosomal | Klinefelter syndrome (XXY) - most common genetic cause; XX sex reversal, XYY |
| Y-chromosome microdeletions | AZFa, AZFb, AZFc (DAZ gene region) - cause azoospermia/severe oligospermia |
| Structural | Sertoli-cell-only syndrome (germ cell aplasia), myotonic dystrophy |
| Cryptorchidism | Undescended testis leads to germ cell deterioration by age 2 |
| Varicocele | Most common surgically correctable cause - causes abnormalities in concentration, motility, and morphology via elevated intratesticular temperature |
| Gonadotoxins | Radiation (>0.1-1.2 Gy impairs spermatogenesis), alkylating chemotherapy drugs, cyclophosphamide |
| Testis injury | Orchitis (mumps), torsion, trauma |
| Systemic disease | Renal failure (uremia), liver cirrhosis, sickle cell disease, diabetes mellitus |
| Idiopathic | ~50% of male infertility - no identifiable cause |
"Varicocele has been described as the most common surgically correctable cause of male subfertility." - Smith and Tanagho's General Urology
C. Posttesticular Causes (Obstructive/Functional)
| Category | Examples |
|---|---|
| Obstruction | Congenital bilateral absence of vas deferens (CBAVD - associated with CFTR mutations), epididymal obstruction, previous vasectomy |
| Ejaculatory dysfunction | Retrograde ejaculation (diabetic neuropathy, post-surgery), anejaculation |
| Immunological | Anti-sperm antibodies (causing agglutination) |
| Sexual dysfunction | Erectile dysfunction, hypospadias, timing/technique issues |
Question 3: Semen Bank (Sperm Banking)
A semen bank (sperm bank) is a facility that collects, processes, freezes, and stores human spermatozoa by cryopreservation for future reproductive use.
Indications for Sperm Banking:
- Before cancer treatment - chemotherapy and radiotherapy cause DNA damage to germ cells and permanent infertility (most common clinical indication)
- Azoospermia - before surgical sperm retrieval (TESE/micro-TESE) for IVF/ICSI
- Occupational hazard exposure (radiation workers, chemical exposure)
- Vasectomy (pre-vasectomy banking as insurance)
- Progressive decline in semen parameters
- Donor insemination - for couples with severe male factor infertility or genetic diseases
Process of Sperm Cryopreservation:
- Collection - ideally 2-3 samples collected 48 hours apart; masturbation after 2-5 days of abstinence
- Analysis - semen analysis performed first to assess quality
- Processing - sperm washed, mixed with cryoprotectant (glycerol or DMSO)
- Freezing - gradual cooling followed by storage in liquid nitrogen at -196°C
- Storage - can be stored indefinitely (viability maintained for decades)
- Thawing and use - for IUI, IVF, or ICSI as needed
Key Notes:
- Not all men can bank sperm - in 12% of men referred for sperm banking, azoospermia or only non-motile sperm are found and cryopreservation cannot be done
- For men who cannot produce semen (stress, severe illness), electro-ejaculation or testicular sperm extraction (TESE) may be used
- Prepubertal boys cannot bank sperm; spermatogonial stem cell banking (experimental) is being studied for them
(Campbell Walsh Wein Urology; Smith and Tanagho's General Urology)
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