Infectious Disease

Pathology · Comprehensive Notes

00 Overview of Infectious Diseases ▾

Definition

Infectious diseases are a group of diseases that are infectious and can cause local or widespread epidemics in the population. They are:

Caused by pathogenic microorganisms
Entering susceptible individuals
Through certain routes of transmission

Causative Agents (Infectious Agents)

Viruses

HIV, HPV, HBV, Influenza

Bacteria

Mycobacterium tuberculosis, Salmonella

Fungi

Candida albicans, Cryptococcus

Protozoa

Plasmodium (malaria)

Helminths

Trichinella spiralis

Ectoparasites

Mites, ticks, spiders

Routes of Transmission

Inhalation

Influenza, SARS, Tuberculosis

Ingestion

Typhoid, Cholera

Sexual Transmission

AIDS, Gonorrhea, Syphilis

Injection / Blood

AIDS, Hepatitis B

Insect Vectors

ZIKA, Dengue fever

Mother to Infant

AIDS, Gonorrhea, Syphilis

Chapter Coverage

Tuberculosis Typhoid Fever Bacterial Enterocolitis / Dysentery Gonorrhea Condyloma (HPV) Syphilis AIDS (HIV)

01 Tuberculosis (TB) ▾

Definition

Tuberculosis is a communicable, chronic, granulomatous disease caused by Mycobacterium tuberculosis.
• Most commonly affects the lungs
• Hallmark pathology: tubercular granulomas with caseous necrosis in the centre

Epidemiology

Leading cause of death from a single infectious agent
~1.7 billion infected; 8–10 million new cases/year; ~2 million deaths/year
Flourishes with poverty, crowding, chronic debilitating illness
High burden: South-East Asia & African Region

Susceptible Persons

Elderly HIV / AIDS Diabetes Chronic Lung Disease Malnutrition Alcoholism Immunosuppressed

Etiology

M. tuberculosis hominis — Most cases
Spread by inhalation (coughing, sneezing, speaking, laughing of active TB person)

M. bovis — Some intestinal TB cases
Spread by drinking contaminated milk

🔬 Staining Tip

Mycobacteria are slender rods, strict aerobes, acid-fast (bind Ziehl-Neelsen / carbol-fuchsin stain → appear pink against blue background). They stubbornly resist decolorization due to high lipid content.

💡 Tuberculin Test (PPD Test)

0.1 mL of PPD injected intracutaneously → read at 48–72 hours → induration ≥5 mm = Positive
⚠️ Positive test only means prior exposure; cannot differentiate infection from disease.

Pathogenesis (Step by Step)

Phase 1 (<3 weeks) — Primary exposure
Bacteria enter macrophage endosomes → inhibit microbicidal responses (via NRAMP1 interference) → unchecked bacillary proliferation → bacteremia → seeding of multiple sites. Patient may be asymptomatic.

↓

Phase 2 (>3 weeks) — Immune response develops
Mycobacterial antigens presented to CD4+ T cells (by macrophages/dendritic cells) via MHC-II → Macrophages secrete IL-12 → TH1 cells activated → secrete IFN-γ → macrophages activated → differentiate into epithelioid cells → form granulomas (hypersensitivity + immunity)

↓

Two outcomes of immune response
Immunity: NO (nitric oxide) + free radicals kill bacteria
Hypersensitivity: Tissue destruction → caseous necrosis, cavitation

Basic Pathological Changes

Change	When it Occurs	Pathological Features
Exudative	Early stage; high virulence; low immunity	Serous / serous-fibrinous inflammation in alveoli
Proliferative (Tubercle)	Less bacteria; low virulence; strong immunity	Formation of tubercles (tubercular granulomas)
Necrosis	Large bacterial load; strong virulence; low resistance	Caseous necrosis — "cheese-like," amorphous, granular, pink

Composition of a Typical Tubercle (MUST KNOW)

Centre: Caseous necrosis (amorphous, granular, pink, structureless)
Middle layer: Epithelioid cells + Langhans giant cells
Periphery: Lymphocytes + proliferating fibroblasts

Epithelioid cells: Activated macrophages, large cells with ill-defined borders, round/oval nucleus, abundant light cytoplasm, resemble epithelial cells

Langhans giant cells: Very large, nuclei arranged in garland / horseshoe pattern at periphery, abundant pink cytoplasm

Transformation of Lesions

↑ Healing (Body resistance wins)

Absorption & dissipation — exudative lesions absorbed via lymphatics
Fibrosis — proliferative lesions & small caseous foci
Calcification — large caseous necrosis → calcified nodule

↓ Worsening (Bacteria win)

Infiltrating progress — exudative lesions appear around old lesion; expands outward
Dissolve & spread — bacilli multiply, caseous necrosis liquefies, bacilli spread via bronchus/lymphatics/blood

Primary Pulmonary Tuberculosis

Develops in a previously unexposed, unsensitized person. More common in children.

Primary Complex (Ghon Complex) = 3 components:

①

Ghon Focus (Primary Tuberculous Focus) Location: lower part of upper lobe or upper part of lower lobe, close to pleura
Size: 1–1.5 cm; gray-white with caseous necrosis in centre

②

Lymph Node Tuberculosis Portopulmonary lymph nodes enlarge and caseate

③

Tuberculous Lymphangitis Disseminated millet-sized lesions between Ghon focus and lymph nodes → dumbbell-shaped shadow on X-ray

Prognosis of Primary TB

~95% of cases: fibrosis + calcification → healing
Some → bronchial lymph node tuberculosis
A few (malnourished, immunocompromised) → miliary tuberculosis

Secondary Pulmonary Tuberculosis

Arises in a previously sensitized host. Can be due to: reactivation of dormant lesions, exogenous reinfection, or shortly after primary TB. Only <5% of primary TB patients develop secondary TB.

Key Features distinguishing from Primary TB:

Location: Apex of upper lobes (bilateral)
Prompt, marked tissue response → localized focus
Cavitation occurs readily; lymph nodes less involved
Inevitable cavitation if neglected → main source of infectivity (open TB)

Patterns of Secondary TB

Focal Pulmonary TB Earliest lesion; <2 cm at apex; dry, firm, gray-white; enclosed by fibrous tissue. Inactive / asymptomatic. Prognosis: mostly heals with fibrosis or calcification; few progress.

Infiltrative Pulmonary TB Develops from focal TB; caseous necrosis enlarges; indefinite borders with inflammatory exudation. Can recover (absorption/fibrosis) or worsen (cavity, hemoptysis, caseous pneumonia).

Caseous Pneumonia Almost whole lobe is consolidated with yellow-white necrosis. Spreads via bronchi. Highly dangerous — much virulent bacilli; poor prognosis; can be fatal if untreated.

Chronic Fibrous-Cavernous Pulmonary TB Multiple thick-walled cavities; pulmonary architecture distorted. Cavity wall (3 layers): Inner = caseous necrosis | Middle = tuberculous granulation tissue | Outer = fibrous connective tissue
Clinical: Hemoptysis (vessel erosion), laryngeal TB, intestinal TB (swallowed sputum), pulmonary heart disease.
⚠️ MAIN SOURCE OF INFECTIVITY (open pulmonary TB; sputum contains bacilli)

Tuberculoma (结核球) Round, 2–5 cm, well-circumscribed by fibrous capsule; caseous necrosis inside; at apex. Latent; anti-TB drugs may not penetrate capsule → may reactivate. Must distinguish from peripheral lung cancer. Surgical ablation preferred.

Tuberculous Pleurisy Pleura involved → serous-fibrinous pleural effusion or proliferating pleurisy.

Miliary Tuberculosis (Hematogenous Spread)

Pulmonary Miliary TB

Organisms drain via lymphatics → lymphatic ducts → right heart → pulmonary arteries
Numerous 2 mm yellow-white round tubercles distributed equally on lung surface and cut surface

Systemic Miliary TB

Foci in lungs seed pulmonary veins → left heart → systemic arteries
Almost every organ can be seeded
Most common sites: liver, spleen, meninges, kidneys

Extra-Pulmonary Tuberculosis

Site	Key Features
Lymph Node	Most common extrapulmonary form. Usually neck ("scrofula"). Nodes enlarge, adhere, cut surface shows yellow-white caseous necrosis.
Intestine	Ring-shaped ulcers on ileum; long axis perpendicular to bowel lumen; shallow, rough edges, uneven base. Secondary = swallowed sputum. Primary (rare) = contaminated milk.
Kidney	Hematogenous spread. Multiple cavities with caseous necrosis. Extends → ureteral TB, hematuria; urine culture positive for AFB.
Vertebra (Pott's Disease)	Vertebral bodies + intervertebral discs destroyed. Forms "cold abscess" — caseous necrosis liquefies, infiltrates paraspinal tissues, without redness, fever, or pain.
Joint	Joint destroyed → fibrosis → ankylosis → loss of motor function.
Other	Meninges (headache, neurological deficits), adrenals, fallopian tubes (infertility), epididymis — all via hematogenous spread.

Primary vs Secondary TB — Comparison Table (EXAM FAVOURITE)

Feature	Primary TB	Secondary TB
Who	Previously unsensitized; children	Previously sensitized host; adults
Location	Lower upper lobe / upper lower lobe (near pleura)	Apex of upper lobe(s)
Ghon Complex	Yes (focus + lymph nodes + lymphangitis)	No; focus is localized
Lymph node involvement	Prominent (caseating hilar nodes)	Less involved
Cavitation	Rare	Common; almost inevitable if neglected
Tissue response	Slow (no prior sensitization)	Prompt, marked (pre-existing hypersensitivity)
Prognosis	95% heal; few → miliary	Variable; can be chronic; major source of infection

Key Terms to Define

Cold Abscess

Caseous necrosis liquefies and infiltrates into paraspinal soft tissues without classic signs of inflammation (no redness, fever, or local pain). Seen in Pott's disease.

Tuberculoma

Round, 2–5 cm, well-encapsulated mass of caseous necrosis at lung apex. Appears as rounded shadow on X-ray. Must be distinguished from peripheral lung cancer.

Primary Complex (Ghon Complex)

Three-component lesion in primary TB: ① Ghon focus ② Portopulmonary lymph node TB ③ Tuberculous lymphangitis between them.

02 Typhoid Fever ▾

Definition & Basics

Typhoid fever is an acute, life-threatening febrile illness caused by Salmonella enterica serotype Typhi.
Inflammation type: Acute proliferative inflammation (macrophages proliferate markedly).

Causative Agent

Salmonella Typhi

Source

Infected patients or asymptomatic carriers

Route

Fecal-oral (contaminated food, water, milk)

Clinical Features

Persistent high fever (39–40°C), splenomegaly, rose-colored spots, relative bradycardia

Pathophysiology

Ingested bacteria travel down GI tract → taken up by mononuclear phagocytes

↓

Bacteria survive & multiply inside cells (incubation 10–14 days)

↓

Discharged into bloodstream → bacteremia + endotoxins → high fever

↓

Move to gallbladder, intestinal lymphoid tissue → inflammation → cholecystitis, intestinal bleeding, perforation

Key Pathological Features

Typhoid Cell: A macrophage that has phagocytized typhoid bacilli, RBCs, lymphocytes, or cell debris.
Typhoid Granuloma: Aggregation of typhoid cells.

Macrophages: large, varied shapes, rich cytoplasm, round/oval nuclei
Typhoid cells aggregate → typhoid granuloma
Lesion mainly in lower ileum (abundant lymphoid tissue there)

4 Stages of Intestinal Changes (Week by Week)

Stage of Swelling Aggregated (Peyer's patches) and isolated lymphatic follicles in ileum swell like gyri; gray-red, soft, uneven mucosa.

Stage of Necrosis Centre of swollen lymphoid tissue undergoes necrosis.

Stage of Ulceration Necrotic tissue sloughs → oval ulcers. Long axis parallel to bowel lumen (vs TB: perpendicular). Severe ulcer → intestinal bleeding and perforation.

Stage of Healing Granulation tissue + epithelium repair the ulcer. No scarring or stricture (vs TB).

Other Organ Involvement

Splenomegaly — due to macrophage proliferation
Liver — swelling and necrosis
Bone marrow — swelling
Other: joints, bones, meninges may be involved

Typhoid vs TB Intestinal Ulcer

Typhoid ulcer — oval; long axis parallel to bowel
TB ulcer — ring-shaped; long axis perpendicular to bowel

03 Bacterial Enterocolitis & Acute Bacillary Dysentery ▾

Bacterial Enterocolitis — Overview

Mechanism 1: Enterotoxin-producing bacteria

Proliferate in gut lumen, elaborate enterotoxins
Secretory toxins (e.g., cholera toxin) → diarrhea without cell damage
Cytotoxins (e.g., Shiga toxin) → direct epithelial necrosis

Mechanism 2: Enteroinvasive bacteria (e.g., Shigella)

Invade mucosal epithelial cells → intracellular proliferation → cell lysis → cell-to-cell spread

Morphology

Damaged surface epithelium with decreased maturation
Hyperemia and edema of lamina propria
Variable neutrophilic infiltration
Severe: erosion, ulceration, submucosal inflammation

Complication: Necrotizing enterocolitis in neonates — part or entire intestine can become hemorrhagic and gangrenous → surgical emergency.

Acute Bacillary Dysentery

Pseudomembranous colitis caused by dysentery bacilli (Shigella).
Route: Fecal-oral transmission. Lesion almost entirely in colon.

Macroscopic (Gross)

Colonic mucosa: erythema, ulceration, pseudomembrane formation
Pseudomembrane: uneven, dirty, gray; partially falls off → "rice bran appearance"
Mucosa congested and edematous

Microscopic (Histological)

Intestinal wall: congestion, edema, neutrophil infiltration
Pseudomembrane composition: superficial mucosa necrosis + exuded fibrin + neutrophils + cellular debris + bacteria

📌 Key: Pseudomembrane

Inflammation type = Pseudomembranous inflammation (NOT granulomatous, NOT serous)

04 Gonorrhea ▾

Definition & Basics

Gonorrhea is a sexually transmitted infection of the lower genitourinary tract caused by Neisseria gonorrhoeae.
Most common reportable communicable disease in the United States.

Causative Agent

Neisseria gonorrhoeae (gram-negative diplococci)

Reservoir

Humans ONLY

Route

Direct contact with mucosa (sexual intercourse)

Mechanism

Attaches to mucosal epithelium → penetrates → invades deeper tissues

Pathology

Provokes intense suppurative (purulent) inflammatory reaction
Gram stain: gram-negative diplococci, many within cytoplasm of neutrophils

Clinical Manifestations

In Males	In Females
Purulent urethral discharge Edematous, congested urethral meatus Ascending: acute prostatitis, epididymitis, orchitis Chronic: urethral stricture → infertility	Often asymptomatic or dysuria, pelvic pain, vaginal discharge Ascending: acute salpingitis, tuboovarian abscess Chronic: scarring of fallopian tubes → infertility

Neonates

Infected via birth canal → ophthalmia neonatorum (purulent eye infection). Prevented by antibiotic eye drops at birth.

Disseminated Infection

Tenosynovitis, arthritis, pustular/hemorrhagic skin lesions. Male homosexuals → pharyngitis or proctitis.

Diagnosis

Culture or nucleic acid amplification techniques (NAAT).

05 Condyloma (Genital Warts / HPV) ▾

Definition & Basics

Condyloma acuminatum is a sexually transmitted disease caused by Human Papillomavirus (HPV), particularly HPV 6 and HPV 11 (low malignant potential).
Most common STD in the US; 4-fold increase in last two decades.

⚠️ Distinguish: Condyloma = HPV 6 and 11 (low risk). HPV 16 and 18 → cervical cancer (high risk — NOT condyloma).

Sites

Males: Penis, around anus

Females: Vulva, cervix, around anus

Moist skin and mucous membranes are vulnerable. Can also occur in axillary fossa.

Pathological Features

Macroscopic

Papillary, distinctly elevated or flat and rugose
Cauliflower-like appearance
Red-pink to pink-brown
Few mm to many cm; single or multiple

Microscopic — KEY FEATURE

Koilocytosis — Hallmark of HPV infection:
• Large cells
• Perinuclear cytoplasmic vacuolization
• Nucleus: irregular, angular, pleomorphic

Association with Neoplasia

HPV → condyloma + vulvar intraepithelial neoplasia (VIN grade I)
VIN I and condyloma (both from low-risk HPV) ≠ VIN II/III (high-risk HPV → cancer)

06 Syphilis ▾

Definition & Basics

Syphilis is a chronic venereal infection caused by the spirochete Treponema pallidum.

Causative Agent

Treponema pallidum (spirochete)

Source

Active cutaneous/mucosal lesion in early-stage partner

Route

Sexual intercourse; transplacental (congenital syphilis)

Staining

Silver stain; dark-field microscopy

Fundamental Pathological Changes (2 Types)

① Proliferative Endarteritis

Endothelial hypertrophy & proliferation → intimal fibrosis → vessel lumen narrowing
Inflammatory infiltrate: plasma cells, lymphocytes, monocytes (plasma cells are characteristic)
Present in ALL stages of syphilis

② Gumma (Syphiloma)

Seen in tertiary syphilis only
Macroscopic: irregular, white-gray/dark red, rubbery
Microscopic: resembles tubercle — incomplete coagulative necrosis in centre (vessel outlines preserved), surrounded by epithelioid cells, plasma cells, lymphocytes. Langhans giant cells rare.
Outcome: absorbed → fibrosis (rarely calcifies)

Stages of Syphilis in Adults

1°

Primary Syphilis Incubation 9–90 days → Chancre at inoculation site.
Features: firm, painless ulcer with well-defined indurated margins and clean moist base.
Histology: lymphocytic + plasmacytic infiltrate + proliferative vascular changes; many spirochetes.
Highly infectious. Resolves in 4–6 weeks. ~25% untreated → secondary syphilis.

2°

Secondary Syphilis ~2 months after chancre resolution.
• Generalized lymphadenopathy (neck + inguinal areas)
• Mucocutaneous lesions (syphilids): symmetrically distributed maculopapular/scaly/pustular rash, including palms and soles
Highly infectious (spirochetes in lesions). Resolves spontaneously → latent phase (~1 year). Can recur.

3°

Tertiary Syphilis Develops in ~1/3 of untreated patients, after latency of ≥5 years.
Spirochetes rarely demonstrable. Three major forms:

Cardiovascular syphilis (80%): Syphilitic aortitis → aortic insufficiency + aortic aneurysm (ascending aorta)
Neurosyphilis (10%): Brain parenchymal disease, Tabes dorsalis
Benign tertiary syphilis: Gummas in bone, skin, mucous membranes, or any organ

Congenital Syphilis

T. pallidum crosses the placenta at any time during pregnancy.

Form	Features
Stillbirth	Hepatomegaly, bone abnormalities, pancreatic fibrosis, pneumonitis
Infantile Syphilis	Chronic rhinitis ("snuffles"), mucocutaneous lesions, visceral & skeletal changes
Late (Tardive) Congenital	Hutchinson's Triad: ① Notched central incisors ② Interstitial keratitis with blindness ③ Deafness (8th cranial nerve injury)

Gumma vs Tubercle — Comparison

Feature	Gumma (Syphilis)	Tubercle (TB)
Disease	Tertiary syphilis	Tuberculosis
Necrosis type	Incomplete coagulative (vessel outlines preserved)	Complete caseous (amorphous, no outlines)
Plasma cells	Prominent	Few
Langhans giant cells	Rare	Characteristic
Calcification	Rare	Common (healing TB)
Organisms	Rarely demonstrable	AFB (in early lesions)

07 AIDS (Acquired Immunodeficiency Syndrome) ▾

Definition

AIDS is a retroviral disease caused by Human Immunodeficiency Virus (HIV).
Characterized by:

Infection and depletion of CD4+ T lymphocytes
Profound immunosuppression leading to opportunistic infections, secondary neoplasms, and neurologic manifestations

⚠️ It is CD4+ (helper T cells) that are depleted — NOT CD8+

Routes of HIV Infection (Epidemiology)

Sexual Transmission — Major route worldwide (>75% of cases) Heterosexual activity accounts for majority globally. Also: male homosexuals.

Parenteral Transmission ① IV drug abusers (largest group) — shared needles/syringes
② Hemophiliacs — factor VIII/IX concentrates
③ Blood transfusion recipients

Mother-to-Infant Transmission In utero (transplacental), intrapartum (during delivery), breast milk.
Transplacental + intrapartum account for most cases.

Pathogenesis

HIV infects T cells and macrophages directly (or carried by Langerhans cells) → replicates in regional lymph nodes → viremia → widespread lymphoid tissue seeding

↓

Host immune response controls viremia → clinical latency phase (can last years)
During latency: viral replication continues; gradual erosion of CD4+ T cells

↓

CD4+ T cell count drops below critical level → full-blown AIDS with susceptibility to opportunistic infections

Macrophage Role in HIV

Macrophages are parasitized early but NOT lysed by HIV. They transport the virus to tissues, particularly the brain (hence CNS involvement).

Clinical Features of AIDS

General

Fever, weight loss, diarrhea, generalized lymphadenopathy

Opportunistic Infections (~80% of deaths)

Pneumocystis jiroveci pneumonia (PCP)
Recurrent mucosal candidiasis
CMV (enteritis, retinitis)
Herpes simplex (ulcerating oral/perianal)
M. tuberculosis + atypical mycobacteria
Cryptococcal meningitis
Cryptosporidium / Isospora diarrhea
S. pneumoniae, H. influenzae infections

Secondary Neoplasms

Kaposi sarcoma (KS)
Non-Hodgkin lymphomas
Cervical cancer (in women)

CNS Involvement

90% at autopsy; 40–60% clinical.
• Aseptic meningitis (at seroconversion)
• Vacuolar myelopathy
• Peripheral neuropathies
• AIDS-dementia complex (most common progressive encephalopathy)
⚠️ CNS may be the SOLE early feature.

HIV + TB Relationship

HIV seropositive status is an important risk factor for development or recrudescence of active tuberculosis
Syphilis is also common in HIV-infected patients
Immunosuppression due to HIV → loss of protection → TB reactivation or new infection

Q&A Quick Review — Tap to Reveal Answers ▾

What type of inflammation is Typhoid fever?

Acute proliferative inflammation (macrophages proliferate). The hallmark cell is the Typhoid cell; clusters form Typhoid granuloma.

What type of inflammation is Bacillary Dysentery?

Pseudomembranous inflammation. Pseudomembrane = superficial mucosa necrosis + fibrin + neutrophils + debris + bacteria.

What is the hallmark pathological feature of TB?

Tubercular granuloma (tubercle) with caseous necrosis in the centre, surrounded by epithelioid cells, Langhans giant cells, lymphocytes, and fibroblasts.

What are the 3 components of a Primary (Ghon) Complex?

① Ghon focus (primary focus in lung) ② Portopulmonary lymph node tuberculosis ③ Tuberculous lymphangitis connecting them.

What is a Cold Abscess?

Caseous necrosis that liquefies and infiltrates paraspinal soft tissues (Pott's disease) WITHOUT classic signs of inflammation — no redness, fever, or pain.

Where is the Ghon focus located?

Lower part of the upper lobe or upper part of the lower lobe, close to the pleura. Size: 1–1.5 cm.

Which HPV types cause condyloma? Which cause cancer?

Condyloma = HPV 6 & 11 (low-risk). Cancer (cervical) = HPV 16 & 18 (high-risk).

What is Koilocytosis?

Hallmark of HPV infection. Large cells with perinuclear cytoplasmic vacuolization and irregular/angular nuclear pleomorphism.

What are the 2 fundamental pathological changes of syphilis?

① Proliferative endarteritis (seen in ALL stages) ② Gumma / syphiloma (seen ONLY in tertiary syphilis).

What is Hutchinson's Triad?

Late congenital syphilis: ① Notched central incisors ② Interstitial keratitis → blindness ③ Deafness (8th cranial nerve injury).

What cells does HIV deplete?

CD4+ T lymphocytes (helper T cells). NOT CD8+. Depletion leads to profound immunosuppression.

What are the 3 routes of HIV transmission?

① Sexual transmission (>75% worldwide) ② Parenteral (IV drug use, blood products) ③ Mother-to-infant (transplacental, intrapartum, breast milk).

Which type of secondary TB is the main source of infectivity?

Chronic fibrous-cavernous pulmonary TB — open pulmonary TB. Sputum contains bacilli; spreads via bronchi to outside.

What is Tuberculoma and how is it treated?

Round 2–5 cm focus of caseous necrosis encapsulated by fibrous tissue at lung apex. Anti-TB drugs don't penetrate well → preferred treatment is surgical ablation. Must distinguish from peripheral lung cancer.

What is the difference between typhoid and TB intestinal ulcers?

Typhoid ulcer: oval; long axis PARALLEL to bowel flow; lower ileum. TB ulcer: ring-shaped; long axis PERPENDICULAR to bowel; shallow, rough edges.

What are the 3 layers of a thick-walled TB cavity?

Inner layer: caseous necrosis. Middle layer: tuberculous granulation tissue. Outer layer: fibrous connective tissue.

KEY Key Terms Glossary ▾

Term	Disease	Definition
Typhoid Cell	Typhoid	Macrophage that has phagocytized typhoid bacilli, RBCs, lymphocytes, or debris
Typhoid Granuloma	Typhoid	Aggregation of typhoid cells
Pseudomembrane	Dysentery	Layer of necrotic mucosa + fibrin + neutrophils + debris + bacteria; forms in pseudomembranous colitis
Koilocytosis	Condyloma / HPV	Perinuclear cytoplasmic vacuolization + nuclear angular pleomorphism; hallmark of HPV
Caseous Necrosis	TB	"Cheese-like" necrosis; amorphous, granular, pink; no cellular outlines; pathognomonic of TB
Ghon Focus	Primary TB	Primary lung focus (1–1.5 cm) at junction of upper and lower lobes near pleura
Primary (Ghon) Complex	Primary TB	Ghon focus + portopulmonary lymph node TB + tuberculous lymphangitis
Tuberculoma	Secondary TB	Well-circumscribed 2–5 cm caseous mass encapsulated by fibrous tissue; latent; needs surgery
Cold Abscess	Spinal TB	Caseous necrosis liquefying into paraspinal tissues without heat/redness/fever/pain
Chancre	Primary Syphilis	Painless indurated ulcer at point of T. pallidum inoculation
Gumma (Syphiloma)	Tertiary Syphilis	Rubbery granulomatous lesion with incomplete coagulative necrosis; only in tertiary syphilis
Hutchinson's Triad	Congenital Syphilis	Notched incisors + interstitial keratitis + deafness
Langhans Giant Cell	TB / Granulomas	Very large cell; nuclei in garland/horseshoe arrangement at periphery; characteristic of TB
Epithelioid Cell	TB	Activated macrophage; resembles epithelial cell; ill-defined borders; most important component of tubercle
Ophthalmia Neonatorum	Gonorrhea	Purulent eye infection in newborns infected via birth canal