1. Definition and epidemiology
2. Causative organisms and vectors
   • Wuchereria bancrofti, Brugia malayi, Brugia timori
3. Life cycle and pathogenesis
4. Clinical features
   • Asymptomatic microfilaremia
   • Acute adenolymphangitis
   • Chronic lymphoedema, elephantiasis, hydrocele
   • Tropical pulmonary eosinophilia
5. Diagnosis
   • Nocturnal blood smear, antigen detection, ultrasound, eosinophilia
6. Treatment
   • Diethylcarbamazine, ivermectin, albendazole, doxycycline
   • Treatment of lymphoedema and hydrocele
7. Prevention and public-health control
   • Mass drug administration, vector control, hygiene and morbidity management
8. Complications, prognosis, and differential diagnosis

Filariasis

Definition

• Wuchereria bancrofti - approximately 90% of global disease
• Brugia malayi
• Brugia timori

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Epidemiology

• It is a neglected tropical disease of tropical and subtropical regions of Asia, Africa, the western Pacific, and parts of the Americas.
• Transmission occurs in areas with suitable mosquito vectors, poor sanitation, standing water, crowding, and inadequate mosquito control.
• Infection is often acquired in childhood, while chronic manifestations commonly appear later in adult life.
• Adult worms may survive for many years in human lymphatics.

Vectors

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Life cycle

1. An infected mosquito bites a human and deposits third-stage larvae (L3) on the skin.
2. Larvae enter through the bite wound and migrate to lymphatic vessels and lymph nodes.
3. They mature into adult male and female worms over months.
4. Adult worms mate in lymphatics and release microfilariae into the bloodstream.
5. A mosquito ingests microfilariae during a blood meal.
6. In the mosquito, microfilariae develop into infective L3 larvae.
7. The next mosquito bite transmits larvae to another person.

Important points

• Definitive host: Human
• Intermediate host/vector: Mosquito
• Infective stage to humans: L3 larva
• Diagnostic stage: Microfilaria in peripheral blood
• Adult worms reside in lymphatic channels, while microfilariae circulate in blood.

Periodicity

• Most W. bancrofti and B. malayi strains are nocturnally periodic, hence blood is collected at night, usually around 10 pm to 2 am.
• Some Pacific strains of W. bancrofti are subperiodic.
• Failure to collect blood at the appropriate time can produce a false-negative smear.

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Pathogenesis

Sequence of events

1. Living or dying worms trigger lymphatic inflammation.
2. Lymphatic vessels dilate and develop endothelial hyperplasia.
3. Lymphocytes, plasma cells, and eosinophils infiltrate lymphatics.
4. Lymphangitis, thrombosis, granuloma formation, and fibrosis develop.
5. Persistent lymphatic obstruction causes chronic lymph stasis.
6. Recurrent bacterial cellulitis and dermatolymphangioadenitis further damage lymphatics.
7. Chronic oedema progresses to fibrosis, skin thickening, hyperkeratosis, and elephantiasis.

Role of Wolbachia

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Clinical features

1. Asymptomatic infection

• Microfilariae in blood
• Circulating filarial antigen
• Subclinical lymphatic damage on imaging
• Mild eosinophilia or no obvious symptoms

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2. Acute filarial disease

Acute adenolymphangitis

• Fever, chills, malaise, myalgia
• Painful lymphadenitis, often inguinal or femoral
• Tender lymphangitis with red, warm overlying skin
• Local oedema
• Recurrent episodes lasting days to about a week

• Funiculitis
• Epididymitis
• Orchitis
• Scrotal pain

Acute dermatolymphangioadenitis

• Sudden fever and chills
• Painful red swollen limb
• Tender lymph nodes
• Lymphangitis
• Skin breakdown or entry lesion

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3. Chronic lymphatic disease

Lymphoedema

• Lower limbs
• Upper limbs, less often
• Breast
• Vulva
• Scrotum

Elephantiasis

• Massive enlargement of the affected part
• Thickened, coarse skin
• Hyperkeratosis
• Papillomatosis
• Deep folds and fissures
• Recurrent cellulitis and fungal infection
• Functional disability, pain, stigma, and psychosocial distress

Hydrocele

• A common chronic manifestation of bancroftian filariasis in men.
• It may be unilateral or bilateral and may become massive.
• It causes discomfort, impaired mobility, sexual and occupational difficulties.
• Definitive treatment is usually hydrocelectomy.

Other manifestations

• Chyluria: milky urine due to rupture of intestinal lymphatics into the urinary tract
• Chylocele
• Chylous ascites
• Pleural effusion
• Lymphatic varices
• Rarely, haematochyluria

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4. Tropical pulmonary eosinophilia

Clinical features

• Paroxysmal nocturnal cough
• Wheeze or bronchospasm, often worse at night
• Low-grade fever
• Dyspnoea
• Weight loss in longstanding disease
• Lymphadenopathy or hepatosplenomegaly in some patients

Investigations

• Marked peripheral eosinophilia
• Very high total IgE
• Elevated antifilarial antibody titre
• Microfilariae generally absent from peripheral blood
• Chest radiograph may show diffuse reticulonodular or miliary infiltrates

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Diagnosis

1. Peripheral blood examination

Thick and thin blood smears

• Collect blood according to microfilarial periodicity.
• In nocturnally periodic infection, collect night blood.
• Thick smear improves detection; thin smear assists species identification.
• Staining is commonly done with Giemsa or Leishman stain.

2. Concentration methods

• Knott concentration technique
• Membrane filtration
• Microhaematocrit tube method

3. Circulating filarial antigen detection

• Immunochromatographic card tests and rapid tests detect circulating antigen of W. bancrofti.
• Helpful because blood can generally be collected at any time.
• Antigen testing does not reliably diagnose Brugia infection.

4. Antibody tests

• Antifilarial antibody assays can support diagnosis in selected cases, especially TPE or amicrofilaraemic disease.
• Limitation: antibodies may indicate past exposure and do not always prove active infection.

5. Eosinophil count and serum IgE

• Eosinophilia may occur during acute disease.
• Marked eosinophilia and raised IgE strongly support TPE but are not specific.

6. Ultrasonography

7. Molecular tests

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Differential diagnosis

For chronic limb lymphoedema

• Primary lymphoedema
• Post-surgical or post-radiotherapy lymphoedema
• Malignancy causing lymphatic obstruction
• Chronic venous insufficiency
• Deep-vein thrombosis
• Podoconiosis
• Lipedema
• Recurrent cellulitis
• Tuberculous lymphadenitis with obstruction

For hydrocele

• Idiopathic hydrocele
• Inguinal hernia
• Epididymo-orchitis
• Testicular tumour
• Trauma
• Tuberculosis

For TPE

• Bronchial asthma
• Allergic bronchopulmonary aspergillosis
• Chronic eosinophilic pneumonia
• Helminthic larva migrans
• Hypereosinophilic syndrome
• Tuberculosis and other causes of chronic pulmonary infiltrates

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Treatment

1. Antifilarial therapy
2. Treatment and prevention of acute bacterial/fungal episodes
3. Long-term morbidity management of lymphoedema and hydrocele

A. Diethylcarbamazine citrate

Action

• Rapidly immobilizes and kills microfilariae.
• Alters their surface, making them more vulnerable to host immune clearance.
• Has partial activity against adult worms.

Usual individual-treatment regimen

• DEC 6 mg/kg/day orally in 3 divided doses for 12 days, commonly after meals.

Adverse effects

• Fever
• Headache
• Malaise
• Myalgia
• Arthralgia
• Rash or urticaria
• Lymphadenitis
• Worsening local inflammation

Important precautions

• Avoid DEC in areas co-endemic for onchocerciasis, because severe inflammatory ocular and systemic reactions may occur.
• In areas with potential high-burden Loa loa infection, treatment requires specialist or public-health guidance because rapid killing of microfilariae can cause severe encephalopathy.
• Reduce dosage in renal impairment.

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B. Ivermectin

• Mainly microfilaricidal.
• It reduces microfilaraemia and transmission.
• It is a key drug in mass drug administration where onchocerciasis is co-endemic.
• It has limited direct activity against adult W. bancrofti worms.

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C. Albendazole

• Used in combination with DEC or ivermectin.
• It has activity against adult worms and may enhance reduction of microfilaraemia.
• It should not be regarded as adequate standalone curative therapy for established individual LF.

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D. Doxycycline

• It may be used in selected individual cases under specialist guidance.
• Avoid in pregnancy and in children younger than 8 years.
• It is generally not used as standard mass drug administration because of the prolonged course and contraindications.

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Management of chronic lymphoedema

Essential limb-care measures

1. Wash the affected limb daily with soap and clean water.
2. Dry carefully, especially between toes and skin folds.
3. Apply emollient to prevent fissures.
4. Treat cuts, ulcers, eczema, fungal infection, and interdigital lesions promptly.
5. Keep nails short and clean.
6. Elevate the affected limb when resting.
7. Perform regular exercise and range-of-motion movements.
8. Use appropriate footwear and avoid trauma.
9. Treat acute bacterial cellulitis promptly with suitable antibiotics.
10. Consider compression therapy only after assessment by a trained clinician, particularly where arterial disease or acute infection is possible.

Hydrocele

• Refer for hydrocelectomy when clinically appropriate.
• Surgery improves mobility, comfort, quality of life, and ability to work.
• Aspiration alone is associated with recurrence and is not definitive management.

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Mass drug administration and public-health control

1. Interrupting transmission through mass drug administration (MDA)
2. Morbidity management and disability prevention for affected persons

WHO-recommended MDA approaches

Vector control

• Elimination of mosquito breeding sites
• Drainage and environmental sanitation
• Larval control where appropriate
• Insecticide-treated bed nets
• Indoor residual spraying in relevant settings
• Personal protection: repellents, screens, long clothing, bed nets

Health education

• Promote MDA participation.
• Educate on daily limb hygiene and early treatment of entry lesions.
• Reduce stigma associated with lymphoedema, elephantiasis, and hydrocele.
• Encourage early medical evaluation of recurrent limb swelling or scrotal enlargement.

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Complications

• Recurrent cellulitis and lymphangitis
• Chronic disability and impaired mobility
• Skin fissures, ulcers, and secondary fungal infection
• Massive hydrocele
• Chyluria and chylous ascites
• Chronic pulmonary fibrosis in untreated TPE
• Social exclusion, anxiety, depression, sexual dysfunction, and loss of income

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Prognosis

• Acute attacks generally resolve but may recur.
• Early infection responds better to antiparasitic therapy.
• Microfilaraemia can be substantially reduced with treatment, decreasing transmission.
• Chronic lymphoedema and elephantiasis are often irreversible once advanced fibrosis has occurred.
• Consistent skin care and prevention of acute bacterial attacks can substantially improve function and prevent worsening.

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Short exam answer: key points

Malaria

Causative species

Life cycle

1. Infected female Anopheles mosquito injects sporozoites into humans.
2. Sporozoites enter hepatocytes and multiply, forming hepatic schizonts.
3. Merozoites are released into blood and invade red cells.
4. Erythrocytic multiplication and red-cell rupture cause febrile paroxysms.
5. Some parasites become gametocytes.
6. A mosquito ingests gametocytes, completing sexual development in the mosquito.

Clinical features

• Fever, often intermittent
• Chills and rigors followed by sweating
• Headache, myalgia, malaise
• Nausea, vomiting
• Anaemia and jaundice
• Splenomegaly and hepatomegaly

1. Cold stage: chills and rigor
2. Hot stage: high fever, headache, vomiting
3. Sweating stage: profuse sweating with fall in temperature

Severe malaria

• Altered consciousness, seizures, or coma: cerebral malaria
• Severe anaemia
• Hypoglycaemia
• Metabolic acidosis or respiratory distress
• Acute kidney injury
• Jaundice with organ dysfunction
• Pulmonary oedema or acute respiratory distress syndrome
• Shock
• Abnormal bleeding
• Haemoglobinuria
• Hyperparasitaemia

Diagnosis

• Peripheral blood smear: thick smear for detection, thin smear for species identification and parasite density
• Rapid diagnostic tests (RDTs): detect parasite antigens
• Complete blood count may show anaemia and thrombocytopenia
• Blood glucose, renal and liver function tests, and acid-base assessment are important in suspected severe malaria

Treatment

• Uncomplicated P. falciparum malaria: artemisinin-based combination therapy (ACT), such as artemether-lumefantrine or another locally recommended ACT.
• Uncomplicated P. vivax or P. ovale malaria: blood-stage treatment plus primaquine or tafenoquine for radical cure of hypnozoites, after testing for glucose-6-phosphate dehydrogenase deficiency.
• Severe malaria: immediate intravenous artesunate, followed by a complete oral ACT once the patient can take oral medicines.

Prevention and control

• Insecticide-treated bed nets
• Indoor residual insecticide spraying
• Elimination of mosquito breeding places
• Prompt diagnosis and complete treatment
• Chemoprophylaxis for eligible travellers
• Intermittent preventive treatment in pregnancy where locally recommended
• Vaccination of eligible children in relevant endemic settings

Key exam points

• P. falciparum causes the most dangerous malaria.
• P. vivax and P. ovale relapse because of liver hypnozoites.
• Peripheral smear is the standard diagnostic test.
• ACT is used for uncomplicated falciparum malaria.
• IV artesunate is the preferred initial treatment for severe malaria.
• Vector control and early case detection are central to prevention.

1. Enteric Fever

Definition

Epidemiology and transmission

• Humans are the only reservoir.
• Spread occurs by the faeco-oral route, through food or water contaminated with stool or urine of infected persons or chronic carriers.
• Common in areas with poor sanitation, unsafe drinking water, and inadequate food hygiene.
• Incubation period: usually 7-14 days, range about 5-21 days.

Pathogenesis

1. Organisms are ingested in contaminated food or water.
2. They invade intestinal mucosa, especially through Peyer patches in the terminal ileum.
3. They multiply in macrophages and spread through lymphatics and blood.
4. Bacteraemia causes sustained fever and systemic toxicity.
5. Reinvasion of intestinal lymphoid tissue causes necrosis and ulceration of Peyer patches.
6. This may result in intestinal haemorrhage or ileal perforation.

Clinical features

First week

• Gradually rising or step-ladder fever
• Headache, malaise, anorexia, myalgia
• Dry cough may occur
• Constipation is common initially, especially in adults
• Relative bradycardia may be present

Second week

• Sustained high fever
• Abdominal pain, distension, tenderness
• Diarrhoea or constipation
• Hepatomegaly and splenomegaly
• Rose spots: faint salmon-pink maculopapular lesions over trunk, seen in some patients
• Toxic appearance, confusion or delirium in severe cases
• Leukopenia may occur

Third week

• Complications may develop if untreated:
  • Intestinal haemorrhage
  • Ileal perforation and peritonitis
  • Encephalopathy
  • Myocarditis
  • Hepatitis
  • Cholecystitis
  • Pneumonia
  • Meningitis, osteomyelitis, or other focal infection

Carrier state

Diagnosis

1. Blood culture

• Best investigation in the first week of illness.
• Culture and antibiotic susceptibility testing are essential because resistance patterns vary geographically.

2. Bone-marrow culture

• Most sensitive test.
• May remain positive even after antibiotic administration.

3. Stool and urine culture

• More likely to become positive in the second and third weeks.
• Also useful in detecting carriers.

4. Serology

• Widal test detects antibodies against O and H antigens.
• It has limited specificity and sensitivity in endemic settings.
• A single Widal titre should not be used alone to diagnose enteric fever.

5. Other laboratory findings

• Leukopenia, relative lymphocytosis
• Anaemia
• Mildly raised liver enzymes
• Thrombocytopenia may occur

Treatment

General measures

• Rest and adequate oral or intravenous fluids
• Paracetamol for fever
• Nutritional support
• Monitor for dehydration, bleeding, abdominal pain, perforation, encephalopathy, and shock

Antibiotics

• Azithromycin for uncomplicated disease in appropriate settings
• Ceftriaxone or another third-generation cephalosporin for severe disease, inability to take oral therapy, or suspected resistant infection
• Carbapenem therapy may be required for extensively drug-resistant disease under specialist advice

Severe enteric fever

Prevention

• Safe water supply and sanitation
• Hand hygiene
• Proper disposal of faeces
• Thorough cooking of food; avoid unsafe street food and unpasteurized products
• Identify and treat carriers
• Vaccination in endemic areas and for eligible travellers

One-line exam summary

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2. Dengue Fever

Definition

Vector and transmission

• Vector: female Aedes aegypti mosquito, and less commonly Aedes albopictus
• Aedes mosquitoes are mainly day-biting
• They breed in clean stagnant water in containers, tyres, flower pots, coolers, tanks, and discarded items.
• Incubation period: usually 4-10 days

Pathogenesis

• Infection with one serotype gives long-term immunity to that serotype.
• A subsequent infection with a different serotype can increase the risk of severe dengue, partly due to antibody-dependent enhancement.
• Severe disease results from increased capillary permeability, plasma leakage, thrombocytopenia, bleeding, and organ dysfunction.

Clinical phases

1. Febrile phase: usually 2-7 days

• Sudden high fever
• Severe headache
• Retro-orbital pain
• Myalgia and arthralgia, called "break-bone fever"
• Nausea and vomiting
• Facial flushing
• Macular or maculopapular rash
• Petechiae or mild mucosal bleeding
• Leukopenia
• Thrombocytopenia may develop

2. Critical phase: around defervescence

• Rising haematocrit
• Rapid fall in platelet count
• Pleural effusion
• Ascites
• Shock
• Respiratory distress
• Bleeding

3. Recovery phase

• Reabsorption of extravasated fluid
• Clinical improvement
• Improving appetite and urine output
• Haematocrit stabilizes
• Platelet count begins to rise
• Convalescent rash may occur

WHO clinical classification

Dengue without warning signs

• Nausea or vomiting
• Rash
• Aches and pains
• Leukopenia
• Positive tourniquet test

Dengue with warning signs

• Severe abdominal pain or tenderness
• Persistent vomiting
• Clinical fluid accumulation, such as ascites or pleural effusion
• Mucosal bleeding
• Lethargy or restlessness
• Liver enlargement greater than 2 cm
• Rising haematocrit with rapidly falling platelet count

Severe dengue

• Severe plasma leakage causing shock or respiratory distress
• Severe bleeding
• Severe organ impairment, such as hepatitis, myocarditis, encephalopathy, renal failure, or markedly raised transaminases

Investigations

During the first 5 days of illness

• NS1 antigen test
• Dengue RT-PCR or nucleic-acid testing where available

After about day 5

• Dengue-specific IgM antibody
• Paired serology may demonstrate a rising antibody titre

Monitoring tests

• Complete blood count:
  • Leukopenia
  • Thrombocytopenia
  • Rising haematocrit suggests plasma leakage
• Liver function tests
• Renal function and electrolytes
• Coagulation profile in bleeding or severe disease
• Chest ultrasound or radiograph when pleural effusion is suspected

Management

Dengue without warning signs

• Oral fluids and oral rehydration
• Paracetamol for fever and pain
• Daily review during febrile and early critical phases
• Monitor warning signs, urine output, haematocrit, and platelet trend
• Advise immediate return if warning signs occur

Dengue with warning signs

• Admit to hospital
• Monitor vital signs, urine output, haematocrit, platelet count, and signs of plasma leakage
• Give carefully titrated isotonic intravenous fluids when indicated

Severe dengue

• Emergency hospital and often intensive-care management
• Prompt, carefully monitored isotonic crystalloid resuscitation
• Assess for shock, bleeding, respiratory distress, and organ failure
• Blood products only when there is significant bleeding or a specific clinical indication, not merely because platelet count is low

Important precautions

• Avoid aspirin, ibuprofen, diclofenac, and other NSAIDs because they increase bleeding risk.
• Avoid unnecessary intramuscular injections.
• Do not give prophylactic platelet transfusions solely for thrombocytopenia in a clinically stable patient.
• Excessive intravenous fluids can cause pulmonary oedema during the recovery phase.

Prevention

• Eliminate mosquito breeding sites weekly
• Cover water-storage containers
• Dispose of tyres, cans, bottles, and other water-holding waste
• Use window screens, repellents, protective clothing, and insecticide-treated measures where appropriate
• Community-based vector control is essential
• Dengue vaccines may be used only according to country-specific recommendations, product indication, age, prior infection status, and local epidemiology

One-line exam summary

1. Chickenpox (Varicella)

Definition

Source and transmission

• Reservoir: humans
• Spread by:
  • Respiratory droplets
  • Direct contact with vesicular fluid
  • Rarely, airborne spread
• A patient is infectious from about 1-2 days before onset of rash until all lesions have crusted.

Incubation period

• Usually 14-16 days
• Range: 10-21 days

Clinical features

Prodrome

• Fever
• Malaise
• Headache
• Loss of appetite

Rash

Macule -> Papule -> Vesicle -> Pustule -> Crust

• Vesicles are classically described as "dew drops on a rose petal."
• Rash starts on the trunk and scalp, then spreads to face and limbs.
• It is mainly centripetal, with more lesions on trunk than extremities.
• Intense pruritus is common.
• Mucosal lesions may occur.

Complications

Common

• Secondary bacterial infection of skin lesions, often due to Staphylococcus aureus or Streptococcus pyogenes
• Scarring

Serious complications

• Varicella pneumonia, especially in adults, smokers, pregnant persons, and immunocompromised patients
• Cerebellar ataxia or encephalitis
• Hepatitis
• Thrombocytopenia
• Glomerulonephritis
• Reye syndrome if aspirin is given to children
• Disseminated or haemorrhagic varicella in immunocompromised persons

Special situations

• Maternal infection in early pregnancy can cause congenital varicella syndrome.
• Perinatal maternal infection may cause severe neonatal varicella.
• VZV remains latent in sensory ganglia and may reactivate later as herpes zoster.

Diagnosis

• PCR from vesicle fluid, scab, or lesion base: preferred
• Direct fluorescent antibody testing
• Serology for immunity assessment, not usually for acute diagnosis

Treatment

Uncomplicated infection in healthy children

• Rest and fluids
• Paracetamol for fever
• Calamine lotion or antihistamine for itching
• Keep nails short to prevent excoriation and secondary infection

Antiviral therapy

• Adults
• Pregnant persons after specialist assessment
• Immunocompromised patients
• Severe or complicated varicella
• Patients with chronic pulmonary or skin disease

Prevention

• Live attenuated varicella vaccine is the main preventive method.
• Susceptible high-risk contacts may require post-exposure prophylaxis with varicella-zoster immunoglobulin or antiviral medication, according to local guidance.
• Isolation until all lesions are crusted.

Exam points

• Cause: Varicella-zoster virus
• Rash: pleomorphic, centripetal, “dew drops on a rose petal”
• Infectious period: 1-2 days before rash until all lesions crust
• Avoid aspirin in children
• Major adult complication: varicella pneumonia
• Prevention: live attenuated varicella vaccine

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2. Measles

Definition

Transmission

• Spread by respiratory droplets and airborne particles.
• The virus can remain infectious in air for a period after an infected person leaves the room.
• Humans are the only reservoir.
• The patient is infectious from about 4 days before to 4 days after rash onset.

Incubation period

• Usually about 10-14 days
• Rash commonly appears around 14 days after exposure.

Clinical features

Prodromal stage

Fever + cough + coryza + conjunctivitis

• High fever
• Malaise
• Photophobia
• Lacrimation

Koplik spots

• Tiny bluish-white spots with surrounding erythema
• Located on buccal mucosa opposite the lower molars
• Appear 1-2 days before rash
• Pathognomonic for measles

Rash

• Erythematous, maculopapular, blanching rash
• Begins on face and behind the ears
• Spreads downward to trunk and limbs
• May become confluent
• Fades in the same order in which it appeared, often with fine desquamation

Complications

Common

• Otitis media
• Diarrhoea
• Laryngotracheobronchitis
• Pneumonia

Serious

• Primary viral pneumonia
• Secondary bacterial pneumonia
• Acute encephalitis
• Acute disseminated encephalomyelitis
• Keratitis and corneal ulceration, particularly in vitamin A deficiency
• Death

Late complication

• Rare progressive neurodegenerative complication
• Occurs years after measles infection
• Presents with cognitive decline, myoclonus, seizures, and progressive neurological deterioration

Diagnosis

• Clinical suspicion in a patient with fever, cough, coryza, conjunctivitis, and a descending maculopapular rash.
• Confirmation by:
  • Measles-specific serum IgM
  • RT-PCR from nasopharyngeal or throat specimen, urine, or blood

Treatment

Supportive care

• Fluids and nutrition
• Antipyretics such as paracetamol
• Treatment of bacterial complications with appropriate antibiotics
• Isolation with airborne precautions

Vitamin A

Prevention

• MMR vaccine is the main preventive measure.
• Two doses are required for reliable protection.
• Susceptible close contacts may receive MMR vaccination soon after exposure where appropriate.
• Immunoglobulin may be indicated for selected high-risk exposed persons, such as infants, pregnant persons without immunity, and severely immunocompromised patients.

Exam points

• Cause: measles virus, a Morbillivirus
• Triad: cough, coryza, conjunctivitis
• Enanthem: Koplik spots
• Rash: starts on face and spreads downward
• Important complications: pneumonia, encephalitis, SSPE
• Prevention: two-dose MMR vaccine

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3. Influenza

Definition

Types of influenza virus

Antigenic variation

Antigenic drift

• Minor mutations in haemagglutinin and neuraminidase genes
• Causes seasonal epidemics
• Explains the need for annual vaccine updates

Antigenic shift

• Major reassortment of influenza A viral gene segments
• Produces a new subtype against which the population has little immunity
• Can cause pandemics

Transmission

• Respiratory droplets
• Aerosols
• Contaminated hands and surfaces followed by inoculation of nose, mouth, or eyes

Incubation period

• Usually 1-4 days, commonly about 2 days

Clinical features

• High fever
• Chills
• Headache
• Severe myalgia and body ache
• Malaise and fatigue
• Dry cough
• Sore throat
• Coryza or nasal congestion

• Vomiting
• Diarrhoea
• Otitis media

Complications

Respiratory

• Primary viral pneumonia
• Secondary bacterial pneumonia, especially due to:
  • Streptococcus pneumoniae
  • Staphylococcus aureus
  • Haemophilus influenzae
• Exacerbation of asthma or COPD
• Acute respiratory distress syndrome

Non-respiratory

• Myocarditis
• Pericarditis
• Encephalitis
• Myositis and rhabdomyolysis
• Febrile seizures in children
• Reye syndrome in children receiving aspirin

High-risk groups

• Young children
• Older adults
• Pregnant persons
• Immunocompromised persons
• Patients with chronic cardiac, pulmonary, renal, liver, neurological, or metabolic disease
• Individuals with obesity

Diagnosis

• Rapid influenza diagnostic tests
• Rapid molecular assays
• RT-PCR, the most sensitive confirmatory method
• Multiplex respiratory viral panels

Treatment

Supportive management

• Rest
• Adequate hydration
• Paracetamol for fever and pain
• Avoid aspirin in children and adolescents

Antiviral drugs

• Oseltamivir
• Zanamivir
• Peramivir

Prevention

• Annual influenza vaccination is the most effective preventive measure.
• Hand hygiene and respiratory etiquette
• Avoiding close contact during illness
• Masking and ventilation measures in high-risk settings
• Antiviral chemoprophylaxis in selected exposed high-risk individuals

Exam points

• Family: Orthomyxoviridae
• Main human types: influenza A and B
• Antigenic drift: seasonal epidemics
• Antigenic shift: influenza A pandemics
• Typical presentation: sudden fever, headache, severe myalgia, dry cough
• Treatment: oseltamivir in severe or high-risk cases
• Prevention: annual influenza vaccination

1. Kala-azar (Visceral Leishmaniasis)

Definition

Agent, vector, and transmission

• Causative organism: Leishmania donovani
• Vector: Female sandfly, Phlebotomus argentipes in India
• Reservoir: Humans are the important reservoir in the Indian subcontinent
• Infective form to humans: Promastigote injected by sandfly
• Diagnostic form in humans: Amastigotes, called Leishman-Donovan bodies, within macrophages

Life cycle

1. Infected female sandfly injects promastigotes during a bite.
2. Promastigotes enter macrophages and convert into amastigotes.
3. Amastigotes multiply within macrophages of the spleen, liver, marrow, and lymph nodes.
4. Another sandfly ingests infected macrophages while feeding.
5. Parasites multiply in the sandfly and develop into infective promastigotes.

Clinical features

Classical triad

Prolonged fever + massive splenomegaly + pancytopenia

• Irregular, prolonged fever
• Weakness, malaise, and weight loss
• Massive splenomegaly, usually more marked than hepatomegaly
• Hepatomegaly
• Anaemia, leukopenia, and thrombocytopenia
• Recurrent infections and bleeding tendency due to cytopenias
• Hypergammaglobulinaemia
• Darkening of skin, especially of face, hands, feet, and abdomen, hence the name kala-azar or “black fever”
• Lymphadenopathy may occur, more often in African disease

Complications

• Severe anaemia
• Secondary bacterial infection
• Haemorrhage due to thrombocytopenia
• Severe malnutrition
• Death if untreated

Post-kala-azar dermal leishmaniasis

• Hypopigmented macules, papules, nodules, or plaques
• Usually begins on face and may spread to trunk and limbs
• Patients can act as reservoirs for transmission in endemic regions

Diagnosis

Clinical suspicion

• Fever for more than 2 weeks
• Splenomegaly
• Weight loss
• Anaemia or pancytopenia

Investigations

1. rK39 rapid diagnostic test
   • Common screening and diagnostic test in endemic settings.
   • Detects anti-leishmanial antibodies.
2. Demonstration of LD bodies
   • Amastigotes in macrophages from splenic aspirate, bone marrow aspirate, or lymph node aspirate.
   • Splenic aspirate is highly sensitive but carries bleeding risk and should be performed only by experienced personnel.
3. Culture and PCR
   • Useful in specialist laboratories.
4. Laboratory findings
   • Pancytopenia
   • Hypergammaglobulinaemia
   • Raised ESR
   • Hypoalbuminaemia

Treatment

• Liposomal amphotericin B: preferred in many settings, including India
• Amphotericin B deoxycholate
• Miltefosine
• Paromomycin
• Sodium stibogluconate in selected regions where susceptibility remains good

Prevention and control

• Early diagnosis and complete treatment
• Active detection of kala-azar and PKDL cases
• Indoor residual insecticide spraying
• Sandfly control and environmental sanitation
• Use of insecticide-treated nets where applicable
• Community awareness in endemic areas

Exam points

• Cause: Leishmania donovani
• Vector: female sandfly
• Classical triad: prolonged fever, splenomegaly, pancytopenia
• Diagnostic form: LD bodies in macrophages
• Rapid test: rK39
• Important sequel: PKDL
• Main treatment: liposomal amphotericin B

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2. Mumps

Definition

Transmission

• Spread by respiratory droplets, saliva, and direct contact with respiratory secretions.
• Humans are the only reservoir.
• Incubation period: usually 16-18 days, range 12-25 days.
• Infectious period: about 2 days before to 5 days after onset of parotid swelling.

Clinical features

Prodrome

• Low-grade fever
• Malaise
• Headache
• Myalgia
• Anorexia

Parotitis

• Painful swelling of one or both parotid glands
• Often bilateral, but may start on one side
• Ear lobe is pushed upward and outward
• Angle of mandible becomes obscured
• Pain on chewing or swallowing, especially sour foods
• Stensen duct may be red and swollen

Complications

In males

• Testicular pain, swelling, and tenderness
• Fever and malaise
• Usually unilateral, occasionally bilateral
• Testicular atrophy may occur
• Permanent infertility is uncommon, even though transient subfertility may occur

In females

• Oophoritis
• Mastitis

Other complications

• Aseptic meningitis
• Encephalitis
• Pancreatitis
• Sensorineural hearing loss, rarely permanent
• Myocarditis
• Nephritis

Diagnosis

• RT-PCR of buccal/oral swab: preferred confirmatory test
• Mumps-specific IgM antibody
• Rising IgG titre in paired serum samples
• CSF examination if meningitis is suspected

Treatment

• Bed rest
• Adequate fluids
• Paracetamol or other suitable analgesic-antipyretic
• Warm or cold compresses for parotid pain
• Soft diet; avoid sour foods that increase salivation
• Scrotal support, rest, analgesia, and cold packs in orchitis

Prevention

• MMR vaccine is the main preventive measure.
• Two doses are used in routine immunization schedules.
• Isolate affected persons for 5 days after onset of parotitis.
• Avoid sharing utensils, cups, or saliva-contaminated items.

Exam points

• Cause: mumps virus, a paramyxovirus
• Transmission: droplets and saliva
• Hallmark: painful parotitis
• Major male complication: orchitis
• Major neurological complication: aseptic meningitis
• Prevention: MMR vaccine

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3. Rabies

Definition

Source and mode of transmission

Reservoirs

• Dogs are the major source of human rabies in many endemic countries.
• Other animals include cats, bats, foxes, jackals, wolves, and monkeys.

Transmission

• Bite of a rabid animal
• Scratch contaminated with saliva
• Lick over broken skin
• Saliva contact with mucous membranes
• Bat exposure

Pathogenesis

1. Virus is inoculated through a bite, scratch, or mucosa.
2. It replicates locally in muscle/connective tissue.
3. It enters peripheral nerves at neuromuscular junctions.
4. It travels centripetally by retrograde axonal transport to the spinal cord and brain.
5. It causes encephalitis.
6. It then spreads centrifugally to salivary glands and other tissues.

Incubation period

• Deep or multiple bites
• Bites on face, head, neck, hands, or fingers
• Heavy viral inoculum
• Young age

Clinical features

1. Prodromal stage

• Fever
• Malaise
• Headache
• Anxiety and irritability
• Nausea and vomiting
• Pain, tingling, burning, or itching at the bite site: highly suggestive feature

2. Acute neurologic stage

Furious rabies

• Hyperactivity and agitation
• Anxiety, confusion, hallucinations
• Hydrophobia: painful pharyngeal spasms on attempting to drink water
• Aerophobia: spasms triggered by air movement
• Hypersalivation
• Autonomic instability
• Alternating periods of agitation and lucidity

Paralytic rabies

• Ascending flaccid paralysis
• May resemble Guillain-Barre syndrome
• Hydrophobia is less prominent
• Progresses to coma and respiratory failure

3. Coma and death

• Coma
• Respiratory paralysis
• Cardiac arrhythmia
• Death usually occurs within days after neurologic symptoms begin

Diagnosis

• RT-PCR on saliva
• PCR or antigen detection in nuchal skin biopsy
• Rabies virus antibodies in serum and CSF
• Corneal impression smears in selected settings

Management of clinical rabies

• Intensive care
• Airway and ventilatory support
• Sedation and analgesia
• Management of autonomic instability
• Psychological support and palliative care when appropriate

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Post-exposure prophylaxis

Immediate wound management

1. Wash and flush the wound thoroughly with soap and running water for at least 15 minutes.
2. Apply a virucidal antiseptic such as povidone-iodine if available.
3. Avoid irritants, tight bandaging, and unnecessary suturing.
4. Give tetanus prophylaxis and antibiotics when clinically indicated.
5. Assess the exposure category and start vaccine promptly when indicated.

WHO exposure categories

Rabies immunoglobulin

• Infiltrate as much as possible into and around all wounds.
• Any remaining calculated volume may be administered away from the vaccine injection site, in line with local policy.
• It should be given as soon as possible with PEP. If unavailable initially, it may be administered within 7 days after the first vaccine dose.

Vaccine

• Start vaccination immediately for category II and III exposure.
• Previously vaccinated persons generally need wound care and abbreviated vaccine booster doses, but no immunoglobulin.
• Never inject rabies vaccine into the gluteal region.

Pre-exposure prophylaxis

• Veterinarians
• Animal handlers
• Laboratory workers handling rabies virus
• Wildlife workers
• Selected travellers or residents in highly endemic remote areas with limited access to PEP

Prevention

• Mass vaccination of dogs
• Control of stray dog populations through humane public-health measures
• Public education on immediate wound washing and urgent medical care after any animal bite
• Pre-exposure vaccination for high-risk groups
• Availability of vaccine and rabies immunoglobulin at treatment centres

Exam points

• Agent: rabies virus, genus Lyssavirus
• Shape: bullet-shaped RNA virus
• Common source in endemic regions: dog
• Cardinal symptoms: hydrophobia and aerophobia
• Once symptomatic: almost always fatal
• PEP: immediate wound washing + vaccine for category II/III + immunoglobulin for category III exposure

1. Poliomyelitis

Definition

Causative agent

• Poliovirus, an enterovirus of the family Picornaviridae
• Three serotypes: poliovirus types 1, 2, and 3
• Wild poliovirus types 2 and 3 have been eradicated; type 1 remains the wild type of concern.

Transmission

• Mainly faeco-oral transmission
• Less commonly through oral-oral spread
• Virus multiplies in the pharynx and intestine and is shed in stool.
• Incubation period: usually 7-14 days, range about 3-35 days.

Pathogenesis

1. Virus enters through mouth.
2. Multiplies in pharynx and intestinal mucosa.
3. Produces viraemia.
4. In a small proportion, virus invades the CNS.
5. It selectively damages anterior horn cells of spinal cord and motor nuclei of brainstem.
6. This results in lower-motor-neuron paralysis.

Clinical forms

1. Inapparent infection

• Most infections are asymptomatic.
• The person may still shed virus and transmit infection.

2. Abortive poliomyelitis

• Mild fever
• Sore throat
• Malaise
• Headache
• Vomiting
• Recovery is complete without CNS involvement.

3. Non-paralytic poliomyelitis

• Aseptic meningitis
• Fever, headache, vomiting
• Neck stiffness
• Back and limb pain
• No paralysis

4. Paralytic poliomyelitis

Spinal poliomyelitis

• Acute, asymmetrical flaccid paralysis
• More common in lower limbs
• Reduced or absent reflexes
• Hypotonia
• No sensory loss
• Muscle wasting develops later

Bulbar poliomyelitis

• Involves cranial nerve nuclei and respiratory centres
• Dysphagia, nasal voice, weak cough
• Respiratory insufficiency
• May be fatal

Bulbospinal poliomyelitis

• Combined spinal and bulbar involvement

Diagnosis

• Clinical suspicion in any child with acute flaccid paralysis (AFP)
• Stool samples for poliovirus culture or RT-PCR
• Two stool samples, collected 24-48 hours apart and as early as possible after onset of paralysis, are used in surveillance.
• CSF may show findings of aseptic meningitis.

Treatment

• Bed rest during acute stage
• Analgesics and antipyretics
• Maintenance of airway and respiratory support when needed
• Management of swallowing difficulty
• Physiotherapy and passive range-of-motion exercises
• Prevention of contractures and deformities
• Orthoses, corrective surgery, and rehabilitation for residual paralysis

Prevention

Vaccines

• OPV: oral polio vaccine, live attenuated
• IPV: inactivated polio vaccine, injectable

Key exam points

• Agent: poliovirus, an enterovirus
• Spread: faeco-oral route
• Site of lesion: anterior horn cells
• Paralysis: asymmetric, flaccid, lower-motor-neuron type, without sensory loss
• Prevention: OPV/IPV and AFP surveillance

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2. Plague

Definition

Causative organism

• Yersinia pestis
• Gram-negative coccobacillus
• Shows bipolar staining, producing a “safety-pin” appearance with special stains.

Reservoir and vector

• Reservoir: wild rodents, such as rats, squirrels, and other small mammals
• Vector: rat flea, especially Xenopsylla cheopis
• Human infection may occur through:
  • Bite of an infected flea
  • Handling infected animals or tissues
  • Inhalation of droplets from a patient or animal with pneumonic plague

Incubation period

Types and clinical features

1. Bubonic plague

• Sudden high fever, chills, severe malaise
• Painful regional lymphadenitis called a bubo
• Bubo is usually inguinal, femoral, axillary, or cervical
• The node is enlarged, tender, and may suppurate
• A flea-bite lesion may be present

2. Septicaemic plague

• Severe sepsis and shock
• Disseminated intravascular coagulation
• Purpura, ecchymoses, and gangrene
• Acral necrosis may cause black discoloration, historically contributing to the term “Black Death”
• Multiorgan failure

3. Pneumonic plague

• Sudden fever and severe toxicity
• Cough, dyspnoea, chest pain
• Haemoptysis or bloody sputum
• Rapid progression to respiratory failure

Diagnosis

• Aspirate from bubo, blood, sputum, or CSF as relevant
• Gram stain or special stains may demonstrate bipolar staining bacilli
• Culture, antigen testing, PCR, or serology in specialist laboratories
• Inform the laboratory if plague is suspected because of biosafety requirements.

Treatment

• Gentamicin
• Streptomycin
• Ciprofloxacin or levofloxacin
• Doxycycline

Prevention and control

• Rodent control and environmental sanitation
• Flea control before rodent destruction
• Avoid handling sick or dead rodents and animals
• Protective measures for persons working with animals in endemic regions
• Droplet precautions for pneumonic plague
• Antibiotic post-exposure prophylaxis for close contacts of pneumonic plague, based on public-health guidance

Key exam points

• Agent: Yersinia pestis
• Vector: rat flea, Xenopsylla cheopis
• Classical lesion: painful bubo
• Most infectious form: pneumonic plague
• Diagnosis: bubo aspirate/culture/PCR
• Treatment: prompt aminoglycoside, fluoroquinolone, or doxycycline-based therapy

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3. Meningitis

Definition

Common causes

Acute bacterial meningitis

Other important types

• Viral meningitis: enteroviruses, mumps virus, herpes viruses
• Tuberculous meningitis: Mycobacterium tuberculosis
• Fungal meningitis: especially Cryptococcus in immunocompromised persons

Pathogenesis of bacterial meningitis

1. Organisms colonize nasopharynx or enter bloodstream from another site.
2. Bacteraemia allows crossing of the blood-brain barrier.
3. Organisms multiply in CSF.
4. Inflammatory cytokines increase permeability of blood-brain barrier.
5. Cerebral oedema, raised intracranial pressure, vasculitis, and impaired cerebral perfusion occur.
6. Untreated disease may rapidly cause coma, shock, and death.

Clinical features

Classical triad

Fever + headache + neck stiffness

• Vomiting
• Photophobia
• Altered sensorium, confusion, or coma
• Seizures
• Irritability or poor feeding in infants
• Positive Kernig or Brudzinski signs
• Focal neurological deficit in complicated disease

Meningococcal meningitis

• Petechial or purpuric rash
• Septicaemia
• Shock
• Disseminated intravascular coagulation
• Waterhouse-Friderichsen syndrome

Diagnosis

Initial investigations

• Blood culture before antibiotics, if this does not delay treatment
• Complete blood count, blood glucose, renal and liver function tests
• Lumbar puncture and CSF examination, if safe
• CSF Gram stain, culture, and PCR where available

When to do CT before lumbar puncture

• Focal neurological deficit
• Papilloedema
• New-onset seizure
• Markedly impaired consciousness
• Known CNS disease
• Severe immunocompromise

CSF findings

Treatment of suspected acute bacterial meningitis

General principles

• Admit urgently.
• Start empiric IV antibiotics immediately.
• Give dexamethasone before or with the first antibiotic dose when appropriate, particularly when pneumococcal meningitis is suspected.
• Treat seizures, shock, hypoxia, and raised intracranial pressure.
• Modify therapy after culture and sensitivity results.

Common empiric approach in adults

• Third-generation cephalosporin, such as ceftriaxone or cefotaxime, plus vancomycin
• Add ampicillin/amoxicillin when Listeria risk is present, for example older age, pregnancy, significant immunosuppression, or certain comorbidities.

Prevention

Vaccination

• Hib vaccine
• Pneumococcal conjugate vaccine
• Meningococcal vaccines

Chemoprophylaxis for meningococcal contacts

Infection control

• Droplet precautions for suspected or confirmed meningococcal meningitis.
• Continue until effective antibiotics have been given for at least 24 hours.

Key exam points

• Meningitis: inflammation of meninges
• Classic triad: fever, headache, neck stiffness
• Most important emergency form: acute bacterial meningitis
• CSF in bacterial meningitis: neutrophils, high protein, low glucose
• Do not delay IV antibiotics for lumbar puncture or CT in a seriously ill patient
• Prevention: Hib, pneumococcal, and meningococcal vaccination

1. Encephalitis

Definition

Causes

Infectious causes

Non-infectious causes

• Autoimmune encephalitis, such as anti-NMDA receptor encephalitis
• Post-infectious encephalomyelitis, for example acute disseminated encephalomyelitis (ADEM)

Pathogenesis

• The organism enters the central nervous system through blood, peripheral nerves, or direct extension.
• Viral replication and host inflammatory response cause cerebral oedema, neuronal injury, haemorrhage, raised intracranial pressure, seizures, and focal deficits.
• HSV classically involves the temporal and frontal lobes.

Clinical features

General manifestations

• Fever and headache
• Altered behaviour, irritability, confusion, delirium, or reduced consciousness
• Seizures
• Nausea and vomiting
• Photophobia
• Neck stiffness may be present if there is associated meningitis

Focal signs

• Aphasia
• Memory disturbance
• Hemiparesis
• Cranial nerve palsies
• Ataxia
• Movement disorders

Features suggesting HSV encephalitis

• Fever with altered mental status
• Personality or behavioural change
• Focal seizures, especially temporal-lobe seizures
• Aphasia or memory impairment
• MRI abnormalities in temporal lobes

Diagnosis

Investigations

• Blood culture, complete blood count, glucose, electrolytes, renal and liver function tests
• Neuroimaging, preferably MRI brain
• Lumbar puncture, if safe
• CSF examination:
  • Cells, protein, glucose
  • Gram stain and bacterial culture
  • HSV PCR and other pathogen-specific PCR tests
• EEG, especially with seizures or suspected temporal-lobe involvement

CSF findings in viral encephalitis

• Lymphocytic pleocytosis
• Mild to moderate protein rise
• Usually normal glucose
• HSV encephalitis may show red blood cells due to haemorrhagic necrosis

Treatment

Immediate management

1. Admit urgently.
2. Stabilize airway, breathing, and circulation.
3. Manage seizures.
4. Control fever and maintain fluids/electrolytes.
5. Monitor for raised intracranial pressure.
6. Start empiric treatment without waiting for confirmation when HSV encephalitis is suspected.

Specific treatment

• IV acyclovir should be started promptly in suspected HSV or VZV encephalitis.
• Appropriate antibiotics are added if bacterial meningitis or meningoencephalitis cannot be excluded.
• Treat tuberculosis, malaria, autoimmune encephalitis, or other identified causes specifically.

Complications

• Persistent epilepsy
• Memory loss and cognitive impairment
• Personality changes
• Motor deficits
• Hearing or visual impairment
• Coma and death

Prevention

• Vaccination against measles, mumps, rubella, varicella, Japanese encephalitis, and rabies where indicated
• Mosquito control and personal protection against mosquito bites
• Early recognition and treatment of infections

Key exam points

• Encephalitis = inflammation of brain tissue.
• Cardinal sign: altered mental status.
• Important treatable cause: HSV encephalitis.
• Diagnosis: MRI brain plus CSF PCR.
• Immediate treatment: IV acyclovir if HSV is suspected.

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2. Chikungunya Fever

Definition

Vector and transmission

• Vector: female Aedes aegypti and Aedes albopictus
• These mosquitoes are mainly day-biting.
• They breed in clean stagnant water in containers, coolers, tyres, flower pots, and tanks.
• Humans are the main amplifying host during outbreaks.
• Incubation period: usually 3-7 days, range 1-12 days.

Clinical features

Acute phase

• Sudden onset high fever
• Severe, symmetrical polyarthralgia or polyarthritis
• Joint swelling and stiffness
• Headache
• Myalgia
• Fatigue
• Maculopapular rash
• Nausea and vomiting
• Conjunctival injection or photophobia in some patients

• Wrists
• Ankles
• Small joints of hands and feet
• Knees
• Elbows

Rash

• Usually maculopapular
• Appears 2-5 days after onset of fever
• May involve trunk, limbs, face, palms, and soles
• Pruritus may occur

Chronic chikungunya arthritis

• Chronic inflammatory polyarthritis
• Morning stiffness
• Tendinitis or tenosynovitis
• Functional limitation
• May mimic rheumatoid arthritis

Complications

• Severe dehydration
• Myocarditis
• Hepatitis
• Uveitis
• Acute kidney injury
• Encephalitis, meningoencephalitis, seizures
• Guillain-Barre syndrome
• Neonatal chikungunya, especially with maternal infection near delivery

Differential diagnosis

• Dengue fever
• Zika virus infection
• Malaria
• Leptospirosis
• Enteric fever
• Acute viral arthritis
• Rheumatoid arthritis

Chikungunya versus dengue

Diagnosis

First week of illness

• RT-PCR for chikungunya viral RNA
• Viral isolation in specialist laboratories

After first week

• Chikungunya-specific IgM antibody test
• Rising IgG titres in paired sera can support diagnosis

Routine tests

• Complete blood count
• Liver and renal function tests when severe illness is suspected
• Test for dengue and malaria where epidemiologically relevant

Treatment

Acute management

• Rest
• Adequate oral fluids
• Paracetamol for fever and pain
• Cold compresses for painful joints
• Monitor vulnerable patients for complications

After dengue has been excluded

• NSAIDs may be used for persistent joint pain if clinically appropriate.
• Persistent arthritis may require physiotherapy, rehabilitation, rheumatology evaluation, and selected anti-inflammatory or disease-modifying treatment under specialist care.

Prevention and control

• Eliminate stagnant water and mosquito breeding containers.
• Cover water storage vessels.
• Use repellents, full-sleeved clothing, screens, and nets.
• Community-based Aedes control is essential.
• Patients should avoid mosquito bites during the first week of illness to reduce onward transmission.

Key exam points

• Agent: chikungunya virus, an alphavirus.
• Vector: Aedes aegypti and Aedes albopictus.
• Hallmark: abrupt fever with severe symmetrical polyarthralgia.
• Chronic complication: persistent inflammatory arthritis.
• Diagnosis: RT-PCR early, IgM later.
• Treatment: supportive; use paracetamol first and exclude dengue before NSAIDs.

HIV/AIDS: Detailed Exam Note

Definition

---

Causative agent

• HIV belongs to the family Retroviridae, subfamily Lentivirinae.
• It is an enveloped, single-stranded RNA retrovirus.
• Two main types:
  • HIV-1: common worldwide and more virulent.
  • HIV-2: mainly found in West Africa; less transmissible and progresses more slowly.

Structure of HIV

---

Modes of transmission

Major routes

1. Sexual transmission
   • Vaginal or anal intercourse without effective barrier protection
   • Risk increases with other sexually transmitted infections, especially genital ulcers.
2. Blood-borne transmission
   • Transfusion of infected blood or blood products
   • Sharing contaminated needles or syringes
   • Unsafe injections
   • Organ transplantation from an infected donor
   • Occupational needle-stick injury
3. Mother-to-child transmission
   • During pregnancy
   • During labour and delivery
   • Through breastfeeding

HIV is not transmitted by

• Handshakes, hugging, sharing food, utensils, toilets, or clothes
• Mosquitoes or other insects
• Saliva, tears, sweat, or casual contact
• Coughing or sneezing

---

Pathogenesis

1. HIV enters the body and binds to the CD4 receptor on T-helper lymphocytes, macrophages, and dendritic cells.
2. Viral gp120 also binds a co-receptor:
   • CCR5, commonly in early infection
   • CXCR4, commonly in later infection
3. Viral RNA is converted to DNA by reverse transcriptase.
4. Viral DNA enters the host nucleus and is integrated into host DNA by integrase.
5. New viral particles are produced and released.
6. Ongoing viral replication and immune activation progressively reduce CD4+ T-cell number and function.
7. Severe CD4 depletion causes opportunistic infections and malignancies.

Consequences of CD4 depletion

• Reduced cell-mediated immunity
• Reduced macrophage activation
• Defective delayed hypersensitivity responses
• Increased risk of tuberculosis, Pneumocystis pneumonia, candidiasis, toxoplasmosis, cryptococcosis, and other opportunistic diseases

---

Natural history of untreated HIV infection

1. Acute HIV infection

• Fever
• Sore throat
• Rash
• Generalized lymphadenopathy
• Myalgia
• Headache
• Oral ulcers
• Diarrhoea
• Aseptic meningitis in some patients

---

2. Clinical latency or chronic HIV infection

• May last for years without antiretroviral therapy.
• The patient may be asymptomatic.
• Persistent generalized lymphadenopathy may occur.
• Viral replication and CD4-cell loss continue despite apparent clinical wellness.

---

3. Symptomatic HIV disease

• Unexplained weight loss
• Persistent fever
• Chronic diarrhoea
• Persistent generalized lymphadenopathy
• Recurrent bacterial infections
• Oral candidiasis
• Herpes zoster
• Recurrent respiratory infections
• Tuberculosis

---

4. AIDS

• A CD4 count below 200 cells/mm³, or
• An AIDS-defining opportunistic infection or malignancy, regardless of CD4 count.

---

Clinical manifestations

Constitutional manifestations

• Fever
• Night sweats
• Weight loss
• Fatigue
• Chronic diarrhoea
• Persistent lymphadenopathy

Dermatological manifestations

• Seborrhoeic dermatitis
• Oral candidiasis
• Herpes zoster
• Recurrent herpes simplex infection
• Molluscum contagiosum
• Pruritic papular eruption
• Kaposi sarcoma
• Bacillary angiomatosis

Oral manifestations

• Oral candidiasis
• Oral hairy leukoplakia
• Recurrent aphthous ulcers
• Periodontal disease
• Recurrent herpes labialis

Respiratory manifestations

• Recurrent bacterial pneumonia
• Tuberculosis
• Pneumocystis jirovecii pneumonia
• Pulmonary cryptococcosis
• Cytomegalovirus pneumonitis, rarely

Gastrointestinal manifestations

• Chronic diarrhoea
• Oesophageal candidiasis
• Cryptosporidiosis
• Isosporiasis
• Cytomegalovirus colitis
• Tuberculosis
• Non-Hodgkin lymphoma

Neurological manifestations

• HIV-associated neurocognitive disorder
• Cryptococcal meningitis
• Toxoplasma encephalitis
• Tuberculous meningitis
• Progressive multifocal leukoencephalopathy
• CMV retinitis with visual loss
• Peripheral neuropathy

---

Opportunistic infections according to CD4 count

---

AIDS-defining conditions

• Pneumocystis jirovecii pneumonia
• Oesophageal candidiasis
• Cryptococcosis outside the lungs
• Toxoplasmosis of brain
• Cytomegalovirus retinitis
• Chronic cryptosporidiosis
• Recurrent bacterial pneumonia
• Recurrent salmonella septicaemia
• Tuberculosis in many clinical staging systems
• Disseminated histoplasmosis
• Kaposi sarcoma
• Invasive cervical carcinoma
• Non-Hodgkin lymphoma
• Primary CNS lymphoma
• HIV wasting syndrome

---

Diagnosis of HIV

1. Screening tests

• HIV-1 and HIV-2 antibodies
• p24 antigen

2. Confirmatory tests

3. Nucleic acid testing

• Suspected acute HIV infection
• Infants born to mothers with HIV
• Indeterminate serology
• Monitoring viral load

4. Baseline assessment after diagnosis

• CD4 count
• HIV viral load
• Complete blood count
• Renal and liver function tests
• Hepatitis B and C screening
• Syphilis and other STI testing
• Tuberculosis screening
• Pregnancy test where relevant
• Evaluation for opportunistic infections
• Resistance testing where available

---

Treatment: Antiretroviral therapy

Principles

• All persons diagnosed with HIV should start ART as soon as possible, regardless of CD4 count.
• ART suppresses viral replication, raises CD4 count, prevents opportunistic disease, improves survival, and prevents sexual transmission when viral suppression is sustained.
• Current ART is highly effective but is not curative because HIV forms a persistent latent reservoir. [Goldman-Cecil Medicine, p. 3584]

Standard first-line ART

Tenofovir + Lamivudine + Dolutegravir
Often abbreviated as TLD

• Tenofovir: nucleoside/nucleotide reverse transcriptase inhibitor
• Lamivudine: nucleoside reverse transcriptase inhibitor
• Dolutegravir: integrase strand-transfer inhibitor

Major antiretroviral drug classes

Monitoring ART

• Adherence assessment at every visit
• Viral load monitoring is the main measure of treatment response
• CD4 monitoring, especially at baseline and in advanced disease
• Monitoring for drug toxicity and interactions
• Evaluation for treatment failure and resistance if viral load remains elevated

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Undetectable = Untransmittable

U = U: Undetectable = Untransmittable

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Treatment of opportunistic infections

Principles

• Diagnose and treat the opportunistic infection promptly.
• Start or optimize ART, with timing tailored to the particular infection.
• Check for drug interactions, especially with rifampicin-containing tuberculosis treatment.
• Prevent recurrence using prophylaxis when indicated.
• Watch for immune reconstitution inflammatory syndrome (IRIS).

IRIS

• Tuberculosis
• Cryptococcosis
• Cytomegalovirus
• Herpes zoster

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Opportunistic infection prophylaxis

---

HIV and tuberculosis

Importance

• HIV increases risk of both primary tuberculosis and reactivation of latent TB.
• TB may present atypically in advanced HIV, including extrapulmonary or disseminated disease.
• All persons with HIV should be screened regularly for TB symptoms.

Management principles

• Treat active TB promptly.
• Start ART during TB treatment, with the timing determined by CD4 count and clinical status.
• Give cotrimoxazole prophylaxis where indicated.
• Consider TB preventive treatment after active TB is excluded.
• Check interactions between rifampicin and ART.

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Prevention of HIV

1. Safe sexual practices

• Correct and consistent condom use
• Testing and treatment for STIs
• Limiting sexual exposure risk
• Partner testing and counselling
• ART with viral suppression for people living with HIV

2. Pre-exposure prophylaxis

• Partners of persons with untreated or unsuppressed HIV
• Persons with recurrent high-risk sexual exposure
• People who inject drugs and share injecting equipment
• Other populations at substantial risk, according to local guidelines

3. Post-exposure prophylaxis

• Start as soon as possible, ideally within hours.
• It should generally be started within 72 hours of exposure.
• A complete course is required under medical guidance.

4. Prevention of mother-to-child transmission

• Routine HIV testing in pregnancy
• Immediate lifelong ART for the pregnant person with HIV
• Viral load monitoring
• Safe delivery planning
• Appropriate infant antiretroviral prophylaxis and HIV testing
• Infant-feeding advice according to local guidelines and availability of safe replacement feeding

5. Blood and injection safety

• Screening of donated blood
• Sterile needles and syringes
• Safe injection practices
• Standard precautions in healthcare settings
• Avoid sharing needles, razors, or other blood-contaminated instruments

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HIV vaccine

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Counselling and psychosocial care

• Confidentiality and non-discrimination
• Adherence counselling
• Partner notification and testing support
• Family-planning and reproductive counselling
• Nutritional assessment
• Screening for depression, substance use, and violence
• Social support and stigma reduction

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Short exam summary

Comparative Table of Infectious Diseases

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Quick Differentiation Points for Exams

Mnemonics for Key Distinguishing Features

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High-yield Differentiation Mnemonics

Dengue vs Chikungunya

“Dengue BLEEDS, Chikungunya BENDS.”

Measles vs Chickenpox

“Measles MARCHES, Chickenpox MIXES.”

• Measles marches from face to trunk to limbs, with lesions of the same stage.
• Chickenpox mixes lesions at multiple stages, macules, papules, vesicles, and crusts, at the same time.

Meningitis vs Encephalitis

“MENINGitis = MENINGES, ENCEPHalitis = ENCEPHALON.”

• Meningitis: fever, headache, neck stiffness, photophobia.
• Encephalitis: fever plus altered consciousness, behavioural change, seizures, or focal neurological deficit.

Polio vs Guillain-Barre syndrome

“POLIO is Patchy; GBS goes Gradually Both Sides.”

• Polio: asymmetric flaccid paralysis, no sensory loss.
• Guillain-Barre syndrome: usually symmetrical ascending weakness, often with sensory symptoms.

Kala-azar vs Malaria

“Kala-azar = Huge spleen + Low all cell lines.”

• Kala-azar: prolonged fever, massive splenomegaly, pancytopenia.
• Malaria: intermittent fever with chills/rigors; malaria parasites detectable in blood.

Rabies vs Tetanus

“Rabies fears water; tetanus locks the jaw.”

• Rabies: hydrophobia, aerophobia, agitation after animal exposure.
• Tetanus: trismus, muscle rigidity, painful spasms, but no hydrophobia.

Filariasis vs Kala-azar

“Filaria blocks lymph; kala-azar fills spleen.”

• Filariasis: lymphoedema, elephantiasis, hydrocele.
• Kala-azar: fever, weight loss, massive spleen, pancytopenia.

HIV/AIDS

“HIV lowers CD4, infections open the door.”

• <200: Pneumocystis jirovecii pneumonia
• <100: Toxoplasmosis, cryptococcosis
• <50: CMV retinitis, disseminated MAC

“200 PJP, 100 Toxo, 50 CMV.”

1. Approach to myopathy: clinical pattern, differential diagnosis, investigations, and general management
2. Muscular dystrophies: Duchenne, Becker, myotonic dystrophy, limb-girdle dystrophies, facioscapulohumeral dystrophy
3. Inflammatory myopathies: polymyositis, dermatomyositis, immune-mediated necrotizing myopathy, inclusion-body myositis
4. Metabolic, endocrine, drug-induced and toxic myopathies
5. Periodic paralysis, mitochondrial myopathies, and congenital myopathies

1. Definition and epidemiology
2. Causative organisms and vectors
   • Wuchereria bancrofti, Brugia malayi, Brugia timori
3. Life cycle and pathogenesis
4. Clinical features
   • Asymptomatic microfilaremia
   • Acute adenolymphangitis
   • Chronic lymphoedema, elephantiasis, hydrocele
   • Tropical pulmonary eosinophilia
5. Diagnosis
   • Nocturnal blood smear, antigen detection, ultrasound, eosinophilia
6. Treatment
   • Diethylcarbamazine, ivermectin, albendazole, doxycycline
   • Treatment of lymphoedema and hydrocele
7. Prevention and public-health control
   • Mass drug administration, vector control, hygiene and morbidity management
8. Complications, prognosis, and differential diagnosis

Definition

• Wuchereria bancrofti - approximately 90% of global disease
• Brugia malayi
• Brugia timori

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Epidemiology

• It is a neglected tropical disease of tropical and subtropical regions of Asia, Africa, the western Pacific, and parts of the Americas.
• Transmission occurs in areas with suitable mosquito vectors, poor sanitation, standing water, crowding, and inadequate mosquito control.
• Infection is often acquired in childhood, while chronic manifestations commonly appear later in adult life.
• Adult worms may survive for many years in human lymphatics.

Vectors

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Life cycle

1. An infected mosquito bites a human and deposits third-stage larvae (L3) on the skin.
2. Larvae enter through the bite wound and migrate to lymphatic vessels and lymph nodes.
3. They mature into adult male and female worms over months.
4. Adult worms mate in lymphatics and release microfilariae into the bloodstream.
5. A mosquito ingests microfilariae during a blood meal.
6. In the mosquito, microfilariae develop into infective L3 larvae.
7. The next mosquito bite transmits larvae to another person.

Important points

• Definitive host: Human
• Intermediate host/vector: Mosquito
• Infective stage to humans: L3 larva
• Diagnostic stage: Microfilaria in peripheral blood
• Adult worms reside in lymphatic channels, while microfilariae circulate in blood.

Periodicity

• Most W. bancrofti and B. malayi strains are nocturnally periodic, hence blood is collected at night, usually around 10 pm to 2 am.
• Some Pacific strains of W. bancrofti are subperiodic.
• Failure to collect blood at the appropriate time can produce a false-negative smear.

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Pathogenesis

Sequence of events

1. Living or dying worms trigger lymphatic inflammation.
2. Lymphatic vessels dilate and develop endothelial hyperplasia.
3. Lymphocytes, plasma cells, and eosinophils infiltrate lymphatics.
4. Lymphangitis, thrombosis, granuloma formation, and fibrosis develop.
5. Persistent lymphatic obstruction causes chronic lymph stasis.
6. Recurrent bacterial cellulitis and dermatolymphangioadenitis further damage lymphatics.
7. Chronic oedema progresses to fibrosis, skin thickening, hyperkeratosis, and elephantiasis.

Role of Wolbachia

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Clinical features

1. Asymptomatic infection

• Microfilariae in blood
• Circulating filarial antigen
• Subclinical lymphatic damage on imaging
• Mild eosinophilia or no obvious symptoms

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2. Acute filarial disease

Acute adenolymphangitis

• Fever, chills, malaise, myalgia
• Painful lymphadenitis, often inguinal or femoral
• Tender lymphangitis with red, warm overlying skin
• Local oedema
• Recurrent episodes lasting days to about a week

• Funiculitis
• Epididymitis
• Orchitis
• Scrotal pain

Acute dermatolymphangioadenitis

• Sudden fever and chills
• Painful red swollen limb
• Tender lymph nodes
• Lymphangitis
• Skin breakdown or entry lesion

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3. Chronic lymphatic disease

Lymphoedema

• Lower limbs
• Upper limbs, less often
• Breast
• Vulva
• Scrotum

Elephantiasis

• Massive enlargement of the affected part
• Thickened, coarse skin
• Hyperkeratosis
• Papillomatosis
• Deep folds and fissures
• Recurrent cellulitis and fungal infection
• Functional disability, pain, stigma, and psychosocial distress

Hydrocele

• A common chronic manifestation of bancroftian filariasis in men.
• It may be unilateral or bilateral and may become massive.
• It causes discomfort, impaired mobility, sexual and occupational difficulties.
• Definitive treatment is usually hydrocelectomy.

Other manifestations

• Chyluria: milky urine due to rupture of intestinal lymphatics into the urinary tract
• Chylocele
• Chylous ascites
• Pleural effusion
• Lymphatic varices
• Rarely, haematochyluria

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4. Tropical pulmonary eosinophilia

Clinical features

• Paroxysmal nocturnal cough
• Wheeze or bronchospasm, often worse at night
• Low-grade fever
• Dyspnoea
• Weight loss in longstanding disease
• Lymphadenopathy or hepatosplenomegaly in some patients

Investigations

• Marked peripheral eosinophilia
• Very high total IgE
• Elevated antifilarial antibody titre
• Microfilariae generally absent from peripheral blood
• Chest radiograph may show diffuse reticulonodular or miliary infiltrates

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Diagnosis

1. Peripheral blood examination

Thick and thin blood smears

• Collect blood according to microfilarial periodicity.
• In nocturnally periodic infection, collect night blood.
• Thick smear improves detection; thin smear assists species identification.
• Staining is commonly done with Giemsa or Leishman stain.

2. Concentration methods

• Knott concentration technique
• Membrane filtration
• Microhaematocrit tube method

3. Circulating filarial antigen detection

• Immunochromatographic card tests and rapid tests detect circulating antigen of W. bancrofti.
• Helpful because blood can generally be collected at any time.
• Antigen testing does not reliably diagnose Brugia infection.

4. Antibody tests

• Antifilarial antibody assays can support diagnosis in selected cases, especially TPE or amicrofilaraemic disease.
• Limitation: antibodies may indicate past exposure and do not always prove active infection.

5. Eosinophil count and serum IgE

• Eosinophilia may occur during acute disease.
• Marked eosinophilia and raised IgE strongly support TPE but are not specific.

6. Ultrasonography

7. Molecular tests

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Differential diagnosis

For chronic limb lymphoedema

• Primary lymphoedema
• Post-surgical or post-radiotherapy lymphoedema
• Malignancy causing lymphatic obstruction
• Chronic venous insufficiency
• Deep-vein thrombosis
• Podoconiosis
• Lipedema
• Recurrent cellulitis
• Tuberculous lymphadenitis with obstruction

For hydrocele

• Idiopathic hydrocele
• Inguinal hernia
• Epididymo-orchitis
• Testicular tumour
• Trauma
• Tuberculosis

For TPE

• Bronchial asthma
• Allergic bronchopulmonary aspergillosis
• Chronic eosinophilic pneumonia
• Helminthic larva migrans
• Hypereosinophilic syndrome
• Tuberculosis and other causes of chronic pulmonary infiltrates

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Treatment

1. Antifilarial therapy
2. Treatment and prevention of acute bacterial/fungal episodes
3. Long-term morbidity management of lymphoedema and hydrocele

A. Diethylcarbamazine citrate

Action

• Rapidly immobilizes and kills microfilariae.
• Alters their surface, making them more vulnerable to host immune clearance.
• Has partial activity against adult worms.

Usual individual-treatment regimen

• DEC 6 mg/kg/day orally in 3 divided doses for 12 days, commonly after meals.

Adverse effects

• Fever
• Headache
• Malaise
• Myalgia
• Arthralgia
• Rash or urticaria
• Lymphadenitis
• Worsening local inflammation

Important precautions

• Avoid DEC in areas co-endemic for onchocerciasis, because severe inflammatory ocular and systemic reactions may occur.
• In areas with potential high-burden Loa loa infection, treatment requires specialist or public-health guidance because rapid killing of microfilariae can cause severe encephalopathy.
• Reduce dosage in renal impairment.

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B. Ivermectin

• Mainly microfilaricidal.
• It reduces microfilaraemia and transmission.
• It is a key drug in mass drug administration where onchocerciasis is co-endemic.
• It has limited direct activity against adult W. bancrofti worms.

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C. Albendazole

• Used in combination with DEC or ivermectin.
• It has activity against adult worms and may enhance reduction of microfilaraemia.
• It should not be regarded as adequate standalone curative therapy for established individual LF.

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D. Doxycycline

• It may be used in selected individual cases under specialist guidance.
• Avoid in pregnancy and in children younger than 8 years.
• It is generally not used as standard mass drug administration because of the prolonged course and contraindications.

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Management of chronic lymphoedema

Essential limb-care measures

1. Wash the affected limb daily with soap and clean water.
2. Dry carefully, especially between toes and skin folds.
3. Apply emollient to prevent fissures.
4. Treat cuts, ulcers, eczema, fungal infection, and interdigital lesions promptly.
5. Keep nails short and clean.
6. Elevate the affected limb when resting.
7. Perform regular exercise and range-of-motion movements.
8. Use appropriate footwear and avoid trauma.
9. Treat acute bacterial cellulitis promptly with suitable antibiotics.
10. Consider compression therapy only after assessment by a trained clinician, particularly where arterial disease or acute infection is possible.

Hydrocele

• Refer for hydrocelectomy when clinically appropriate.
• Surgery improves mobility, comfort, quality of life, and ability to work.
• Aspiration alone is associated with recurrence and is not definitive management.

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Mass drug administration and public-health control

1. Interrupting transmission through mass drug administration (MDA)
2. Morbidity management and disability prevention for affected persons

WHO-recommended MDA approaches

Vector control

• Elimination of mosquito breeding sites
• Drainage and environmental sanitation
• Larval control where appropriate
• Insecticide-treated bed nets
• Indoor residual spraying in relevant settings
• Personal protection: repellents, screens, long clothing, bed nets

Health education

• Promote MDA participation.
• Educate on daily limb hygiene and early treatment of entry lesions.
• Reduce stigma associated with lymphoedema, elephantiasis, and hydrocele.
• Encourage early medical evaluation of recurrent limb swelling or scrotal enlargement.

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Complications

• Recurrent cellulitis and lymphangitis
• Chronic disability and impaired mobility
• Skin fissures, ulcers, and secondary fungal infection
• Massive hydrocele
• Chyluria and chylous ascites
• Chronic pulmonary fibrosis in untreated TPE
• Social exclusion, anxiety, depression, sexual dysfunction, and loss of income

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Prognosis

• Acute attacks generally resolve but may recur.
• Early infection responds better to antiparasitic therapy.
• Microfilaraemia can be substantially reduced with treatment, decreasing transmission.
• Chronic lymphoedema and elephantiasis are often irreversible once advanced fibrosis has occurred.
• Consistent skin care and prevention of acute bacterial attacks can substantially improve function and prevent worsening.

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Short exam answer: key points

Causative species

Life cycle

1. Infected female Anopheles mosquito injects sporozoites into humans.
2. Sporozoites enter hepatocytes and multiply, forming hepatic schizonts.
3. Merozoites are released into blood and invade red cells.
4. Erythrocytic multiplication and red-cell rupture cause febrile paroxysms.
5. Some parasites become gametocytes.
6. A mosquito ingests gametocytes, completing sexual development in the mosquito.

Clinical features

• Fever, often intermittent
• Chills and rigors followed by sweating
• Headache, myalgia, malaise
• Nausea, vomiting
• Anaemia and jaundice
• Splenomegaly and hepatomegaly

1. Cold stage: chills and rigor
2. Hot stage: high fever, headache, vomiting
3. Sweating stage: profuse sweating with fall in temperature

Severe malaria

• Altered consciousness, seizures, or coma: cerebral malaria
• Severe anaemia
• Hypoglycaemia
• Metabolic acidosis or respiratory distress
• Acute kidney injury
• Jaundice with organ dysfunction
• Pulmonary oedema or acute respiratory distress syndrome
• Shock
• Abnormal bleeding
• Haemoglobinuria
• Hyperparasitaemia

Diagnosis

• Peripheral blood smear: thick smear for detection, thin smear for species identification and parasite density
• Rapid diagnostic tests (RDTs): detect parasite antigens
• Complete blood count may show anaemia and thrombocytopenia
• Blood glucose, renal and liver function tests, and acid-base assessment are important in suspected severe malaria

Treatment

• Uncomplicated P. falciparum malaria: artemisinin-based combination therapy (ACT), such as artemether-lumefantrine or another locally recommended ACT.
• Uncomplicated P. vivax or P. ovale malaria: blood-stage treatment plus primaquine or tafenoquine for radical cure of hypnozoites, after testing for glucose-6-phosphate dehydrogenase deficiency.
• Severe malaria: immediate intravenous artesunate, followed by a complete oral ACT once the patient can take oral medicines.

Prevention and control

• Insecticide-treated bed nets
• Indoor residual insecticide spraying
• Elimination of mosquito breeding places
• Prompt diagnosis and complete treatment
• Chemoprophylaxis for eligible travellers
• Intermittent preventive treatment in pregnancy where locally recommended
• Vaccination of eligible children in relevant endemic settings

Key exam points

• P. falciparum causes the most dangerous malaria.
• P. vivax and P. ovale relapse because of liver hypnozoites.
• Peripheral smear is the standard diagnostic test.
• ACT is used for uncomplicated falciparum malaria.
• IV artesunate is the preferred initial treatment for severe malaria.
• Vector control and early case detection are central to prevention.# 1. Enteric Fever

Definition

Epidemiology and transmission

• Humans are the only reservoir.
• Spread occurs by the faeco-oral route, through food or water contaminated with stool or urine of infected persons or chronic carriers.
• Common in areas with poor sanitation, unsafe drinking water, and inadequate food hygiene.
• Incubation period: usually 7-14 days, range about 5-21 days.

Pathogenesis

1. Organisms are ingested in contaminated food or water.
2. They invade intestinal mucosa, especially through Peyer patches in the terminal ileum.
3. They multiply in macrophages and spread through lymphatics and blood.
4. Bacteraemia causes sustained fever and systemic toxicity.
5. Reinvasion of intestinal lymphoid tissue causes necrosis and ulceration of Peyer patches.
6. This may result in intestinal haemorrhage or ileal perforation.

Clinical features

First week

• Gradually rising or step-ladder fever
• Headache, malaise, anorexia, myalgia
• Dry cough may occur
• Constipation is common initially, especially in adults
• Relative bradycardia may be present

Second week

• Sustained high fever
• Abdominal pain, distension, tenderness
• Diarrhoea or constipation
• Hepatomegaly and splenomegaly
• Rose spots: faint salmon-pink maculopapular lesions over trunk, seen in some patients
• Toxic appearance, confusion or delirium in severe cases
• Leukopenia may occur

Third week

• Complications may develop if untreated:
  • Intestinal haemorrhage
  • Ileal perforation and peritonitis
  • Encephalopathy
  • Myocarditis
  • Hepatitis
  • Cholecystitis
  • Pneumonia
  • Meningitis, osteomyelitis, or other focal infection

Carrier state

Diagnosis

1. Blood culture

• Best investigation in the first week of illness.
• Culture and antibiotic susceptibility testing are essential because resistance patterns vary geographically.

2. Bone-marrow culture

• Most sensitive test.
• May remain positive even after antibiotic administration.

3. Stool and urine culture

• More likely to become positive in the second and third weeks.
• Also useful in detecting carriers.

4. Serology

• Widal test detects antibodies against O and H antigens.
• It has limited specificity and sensitivity in endemic settings.
• A single Widal titre should not be used alone to diagnose enteric fever.

5. Other laboratory findings

• Leukopenia, relative lymphocytosis
• Anaemia
• Mildly raised liver enzymes
• Thrombocytopenia may occur

Treatment

General measures

• Rest and adequate oral or intravenous fluids
• Paracetamol for fever
• Nutritional support
• Monitor for dehydration, bleeding, abdominal pain, perforation, encephalopathy, and shock

Antibiotics

• Azithromycin for uncomplicated disease in appropriate settings
• Ceftriaxone or another third-generation cephalosporin for severe disease, inability to take oral therapy, or suspected resistant infection
• Carbapenem therapy may be required for extensively drug-resistant disease under specialist advice

Severe enteric fever

Prevention

• Safe water supply and sanitation
• Hand hygiene
• Proper disposal of faeces
• Thorough cooking of food; avoid unsafe street food and unpasteurized products
• Identify and treat carriers
• Vaccination in endemic areas and for eligible travellers

One-line exam summary

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2. Dengue Fever

Definition

Vector and transmission

• Vector: female Aedes aegypti mosquito, and less commonly Aedes albopictus
• Aedes mosquitoes are mainly day-biting
• They breed in clean stagnant water in containers, tyres, flower pots, coolers, tanks, and discarded items.
• Incubation period: usually 4-10 days

Pathogenesis

• Infection with one serotype gives long-term immunity to that serotype.
• A subsequent infection with a different serotype can increase the risk of severe dengue, partly due to antibody-dependent enhancement.
• Severe disease results from increased capillary permeability, plasma leakage, thrombocytopenia, bleeding, and organ dysfunction.

Clinical phases

1. Febrile phase: usually 2-7 days

• Sudden high fever
• Severe headache
• Retro-orbital pain
• Myalgia and arthralgia, called "break-bone fever"
• Nausea and vomiting
• Facial flushing
• Macular or maculopapular rash
• Petechiae or mild mucosal bleeding
• Leukopenia
• Thrombocytopenia may develop

2. Critical phase: around defervescence

• Rising haematocrit
• Rapid fall in platelet count
• Pleural effusion
• Ascites
• Shock
• Respiratory distress
• Bleeding

3. Recovery phase

• Reabsorption of extravasated fluid
• Clinical improvement
• Improving appetite and urine output
• Haematocrit stabilizes
• Platelet count begins to rise
• Convalescent rash may occur

WHO clinical classification

Dengue without warning signs

• Nausea or vomiting
• Rash
• Aches and pains
• Leukopenia
• Positive tourniquet test

Dengue with warning signs

• Severe abdominal pain or tenderness
• Persistent vomiting
• Clinical fluid accumulation, such as ascites or pleural effusion
• Mucosal bleeding
• Lethargy or restlessness
• Liver enlargement greater than 2 cm
• Rising haematocrit with rapidly falling platelet count

Severe dengue

• Severe plasma leakage causing shock or respiratory distress
• Severe bleeding
• Severe organ impairment, such as hepatitis, myocarditis, encephalopathy, renal failure, or markedly raised transaminases

Investigations

During the first 5 days of illness

• NS1 antigen test
• Dengue RT-PCR or nucleic-acid testing where available

After about day 5

• Dengue-specific IgM antibody
• Paired serology may demonstrate a rising antibody titre

Monitoring tests

• Complete blood count:
  • Leukopenia
  • Thrombocytopenia
  • Rising haematocrit suggests plasma leakage
• Liver function tests
• Renal function and electrolytes
• Coagulation profile in bleeding or severe disease
• Chest ultrasound or radiograph when pleural effusion is suspected

Management

Dengue without warning signs

• Oral fluids and oral rehydration
• Paracetamol for fever and pain
• Daily review during febrile and early critical phases
• Monitor warning signs, urine output, haematocrit, and platelet trend
• Advise immediate return if warning signs occur

Dengue with warning signs

• Admit to hospital
• Monitor vital signs, urine output, haematocrit, platelet count, and signs of plasma leakage
• Give carefully titrated isotonic intravenous fluids when indicated

Severe dengue

• Emergency hospital and often intensive-care management
• Prompt, carefully monitored isotonic crystalloid resuscitation
• Assess for shock, bleeding, respiratory distress, and organ failure
• Blood products only when there is significant bleeding or a specific clinical indication, not merely because platelet count is low

Important precautions

• Avoid aspirin, ibuprofen, diclofenac, and other NSAIDs because they increase bleeding risk.
• Avoid unnecessary intramuscular injections.
• Do not give prophylactic platelet transfusions solely for thrombocytopenia in a clinically stable patient.
• Excessive intravenous fluids can cause pulmonary oedema during the recovery phase.

Prevention

• Eliminate mosquito breeding sites weekly
• Cover water-storage containers
• Dispose of tyres, cans, bottles, and other water-holding waste
• Use window screens, repellents, protective clothing, and insecticide-treated measures where appropriate
• Community-based vector control is essential
• Dengue vaccines may be used only according to country-specific recommendations, product indication, age, prior infection status, and local epidemiology

One-line exam summary

Definition

Source and transmission

• Reservoir: humans
• Spread by:
  • Respiratory droplets
  • Direct contact with vesicular fluid
  • Rarely, airborne spread
• A patient is infectious from about 1-2 days before onset of rash until all lesions have crusted.

Incubation period

• Usually 14-16 days
• Range: 10-21 days

Clinical features

Prodrome

• Fever
• Malaise
• Headache
• Loss of appetite

Rash

Macule -> Papule -> Vesicle -> Pustule -> Crust

• Vesicles are classically described as "dew drops on a rose petal."
• Rash starts on the trunk and scalp, then spreads to face and limbs.
• It is mainly centripetal, with more lesions on trunk than extremities.
• Intense pruritus is common.
• Mucosal lesions may occur.

Complications

Common

• Secondary bacterial infection of skin lesions, often due to Staphylococcus aureus or Streptococcus pyogenes
• Scarring

Serious complications

• Varicella pneumonia, especially in adults, smokers, pregnant persons, and immunocompromised patients
• Cerebellar ataxia or encephalitis
• Hepatitis
• Thrombocytopenia
• Glomerulonephritis
• Reye syndrome if aspirin is given to children
• Disseminated or haemorrhagic varicella in immunocompromised persons

Special situations

• Maternal infection in early pregnancy can cause congenital varicella syndrome.
• Perinatal maternal infection may cause severe neonatal varicella.
• VZV remains latent in sensory ganglia and may reactivate later as herpes zoster.

Diagnosis

• PCR from vesicle fluid, scab, or lesion base: preferred
• Direct fluorescent antibody testing
• Serology for immunity assessment, not usually for acute diagnosis

Treatment

Uncomplicated infection in healthy children

• Rest and fluids
• Paracetamol for fever
• Calamine lotion or antihistamine for itching
• Keep nails short to prevent excoriation and secondary infection

Antiviral therapy

• Adults
• Pregnant persons after specialist assessment
• Immunocompromised patients
• Severe or complicated varicella
• Patients with chronic pulmonary or skin disease

Prevention

• Live attenuated varicella vaccine is the main preventive method.
• Susceptible high-risk contacts may require post-exposure prophylaxis with varicella-zoster immunoglobulin or antiviral medication, according to local guidance.
• Isolation until all lesions are crusted.

Exam points

• Cause: Varicella-zoster virus
• Rash: pleomorphic, centripetal, “dew drops on a rose petal”
• Infectious period: 1-2 days before rash until all lesions crust
• Avoid aspirin in children
• Major adult complication: varicella pneumonia
• Prevention: live attenuated varicella vaccine

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2. Measles

Definition

Transmission

• Spread by respiratory droplets and airborne particles.
• The virus can remain infectious in air for a period after an infected person leaves the room.
• Humans are the only reservoir.
• The patient is infectious from about 4 days before to 4 days after rash onset.

Incubation period

• Usually about 10-14 days
• Rash commonly appears around 14 days after exposure.

Clinical features

Prodromal stage

Fever + cough + coryza + conjunctivitis

• High fever
• Malaise
• Photophobia
• Lacrimation

Koplik spots

• Tiny bluish-white spots with surrounding erythema
• Located on buccal mucosa opposite the lower molars
• Appear 1-2 days before rash
• Pathognomonic for measles

Rash

• Erythematous, maculopapular, blanching rash
• Begins on face and behind the ears
• Spreads downward to trunk and limbs
• May become confluent
• Fades in the same order in which it appeared, often with fine desquamation

Complications

Common

• Otitis media
• Diarrhoea
• Laryngotracheobronchitis
• Pneumonia

Serious

• Primary viral pneumonia
• Secondary bacterial pneumonia
• Acute encephalitis
• Acute disseminated encephalomyelitis
• Keratitis and corneal ulceration, particularly in vitamin A deficiency
• Death

Late complication

• Rare progressive neurodegenerative complication
• Occurs years after measles infection
• Presents with cognitive decline, myoclonus, seizures, and progressive neurological deterioration

Diagnosis

• Clinical suspicion in a patient with fever, cough, coryza, conjunctivitis, and a descending maculopapular rash.
• Confirmation by:
  • Measles-specific serum IgM
  • RT-PCR from nasopharyngeal or throat specimen, urine, or blood

Treatment

Supportive care

• Fluids and nutrition
• Antipyretics such as paracetamol
• Treatment of bacterial complications with appropriate antibiotics
• Isolation with airborne precautions

Vitamin A

Prevention

• MMR vaccine is the main preventive measure.
• Two doses are required for reliable protection.
• Susceptible close contacts may receive MMR vaccination soon after exposure where appropriate.
• Immunoglobulin may be indicated for selected high-risk exposed persons, such as infants, pregnant persons without immunity, and severely immunocompromised patients.

Exam points

• Cause: measles virus, a Morbillivirus
• Triad: cough, coryza, conjunctivitis
• Enanthem: Koplik spots
• Rash: starts on face and spreads downward
• Important complications: pneumonia, encephalitis, SSPE
• Prevention: two-dose MMR vaccine

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3. Influenza

Definition

Types of influenza virus

Antigenic variation

Antigenic drift

• Minor mutations in haemagglutinin and neuraminidase genes
• Causes seasonal epidemics
• Explains the need for annual vaccine updates

Antigenic shift

• Major reassortment of influenza A viral gene segments
• Produces a new subtype against which the population has little immunity
• Can cause pandemics

Transmission

• Respiratory droplets
• Aerosols
• Contaminated hands and surfaces followed by inoculation of nose, mouth, or eyes

Incubation period

• Usually 1-4 days, commonly about 2 days

Clinical features

• High fever
• Chills
• Headache
• Severe myalgia and body ache
• Malaise and fatigue
• Dry cough
• Sore throat
• Coryza or nasal congestion

• Vomiting
• Diarrhoea
• Otitis media

Complications

Respiratory

• Primary viral pneumonia
• Secondary bacterial pneumonia, especially due to:
  • Streptococcus pneumoniae
  • Staphylococcus aureus
  • Haemophilus influenzae
• Exacerbation of asthma or COPD
• Acute respiratory distress syndrome

Non-respiratory

• Myocarditis
• Pericarditis
• Encephalitis
• Myositis and rhabdomyolysis
• Febrile seizures in children
• Reye syndrome in children receiving aspirin

High-risk groups

• Young children
• Older adults
• Pregnant persons
• Immunocompromised persons
• Patients with chronic cardiac, pulmonary, renal, liver, neurological, or metabolic disease
• Individuals with obesity

Diagnosis

• Rapid influenza diagnostic tests
• Rapid molecular assays
• RT-PCR, the most sensitive confirmatory method
• Multiplex respiratory viral panels

Treatment

Supportive management

• Rest
• Adequate hydration
• Paracetamol for fever and pain
• Avoid aspirin in children and adolescents

Antiviral drugs

• Oseltamivir
• Zanamivir
• Peramivir

Prevention

• Annual influenza vaccination is the most effective preventive measure.
• Hand hygiene and respiratory etiquette
• Avoiding close contact during illness
• Masking and ventilation measures in high-risk settings
• Antiviral chemoprophylaxis in selected exposed high-risk individuals

Exam points

• Family: Orthomyxoviridae
• Main human types: influenza A and B
• Antigenic drift: seasonal epidemics
• Antigenic shift: influenza A pandemics
• Typical presentation: sudden fever, headache, severe myalgia, dry cough
• Treatment: oseltamivir in severe or high-risk cases
• Prevention: annual influenza vaccination# 1. Kala-azar (Visceral Leishmaniasis)

Definition

Agent, vector, and transmission

• Causative organism: Leishmania donovani
• Vector: Female sandfly, Phlebotomus argentipes in India
• Reservoir: Humans are the important reservoir in the Indian subcontinent
• Infective form to humans: Promastigote injected by sandfly
• Diagnostic form in humans: Amastigotes, called Leishman-Donovan bodies, within macrophages

Life cycle

1. Infected female sandfly injects promastigotes during a bite.
2. Promastigotes enter macrophages and convert into amastigotes.
3. Amastigotes multiply within macrophages of the spleen, liver, marrow, and lymph nodes.
4. Another sandfly ingests infected macrophages while feeding.
5. Parasites multiply in the sandfly and develop into infective promastigotes.

Clinical features

Classical triad

Prolonged fever + massive splenomegaly + pancytopenia

• Irregular, prolonged fever
• Weakness, malaise, and weight loss
• Massive splenomegaly, usually more marked than hepatomegaly
• Hepatomegaly
• Anaemia, leukopenia, and thrombocytopenia
• Recurrent infections and bleeding tendency due to cytopenias
• Hypergammaglobulinaemia
• Darkening of skin, especially of face, hands, feet, and abdomen, hence the name kala-azar or “black fever”
• Lymphadenopathy may occur, more often in African disease

Complications

• Severe anaemia
• Secondary bacterial infection
• Haemorrhage due to thrombocytopenia
• Severe malnutrition
• Death if untreated

Post-kala-azar dermal leishmaniasis

• Hypopigmented macules, papules, nodules, or plaques
• Usually begins on face and may spread to trunk and limbs
• Patients can act as reservoirs for transmission in endemic regions

Diagnosis

Clinical suspicion

• Fever for more than 2 weeks
• Splenomegaly
• Weight loss
• Anaemia or pancytopenia

Investigations

1. rK39 rapid diagnostic test
   • Common screening and diagnostic test in endemic settings.
   • Detects anti-leishmanial antibodies.
2. Demonstration of LD bodies
   • Amastigotes in macrophages from splenic aspirate, bone marrow aspirate, or lymph node aspirate.
   • Splenic aspirate is highly sensitive but carries bleeding risk and should be performed only by experienced personnel.
3. Culture and PCR
   • Useful in specialist laboratories.
4. Laboratory findings
   • Pancytopenia
   • Hypergammaglobulinaemia
   • Raised ESR
   • Hypoalbuminaemia

Treatment

• Liposomal amphotericin B: preferred in many settings, including India
• Amphotericin B deoxycholate
• Miltefosine
• Paromomycin
• Sodium stibogluconate in selected regions where susceptibility remains good

Prevention and control

• Early diagnosis and complete treatment
• Active detection of kala-azar and PKDL cases
• Indoor residual insecticide spraying
• Sandfly control and environmental sanitation
• Use of insecticide-treated nets where applicable
• Community awareness in endemic areas

Exam points

• Cause: Leishmania donovani
• Vector: female sandfly
• Classical triad: prolonged fever, splenomegaly, pancytopenia
• Diagnostic form: LD bodies in macrophages
• Rapid test: rK39
• Important sequel: PKDL
• Main treatment: liposomal amphotericin B

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2. Mumps

Definition

Transmission

• Spread by respiratory droplets, saliva, and direct contact with respiratory secretions.
• Humans are the only reservoir.
• Incubation period: usually 16-18 days, range 12-25 days.
• Infectious period: about 2 days before to 5 days after onset of parotid swelling.

Clinical features

Prodrome

• Low-grade fever
• Malaise
• Headache
• Myalgia
• Anorexia

Parotitis

• Painful swelling of one or both parotid glands
• Often bilateral, but may start on one side
• Ear lobe is pushed upward and outward
• Angle of mandible becomes obscured
• Pain on chewing or swallowing, especially sour foods
• Stensen duct may be red and swollen

Complications

In males

• Testicular pain, swelling, and tenderness
• Fever and malaise
• Usually unilateral, occasionally bilateral
• Testicular atrophy may occur
• Permanent infertility is uncommon, even though transient subfertility may occur

In females

• Oophoritis
• Mastitis

Other complications

• Aseptic meningitis
• Encephalitis
• Pancreatitis
• Sensorineural hearing loss, rarely permanent
• Myocarditis
• Nephritis

Diagnosis

• RT-PCR of buccal/oral swab: preferred confirmatory test
• Mumps-specific IgM antibody
• Rising IgG titre in paired serum samples
• CSF examination if meningitis is suspected

Treatment

• Bed rest
• Adequate fluids
• Paracetamol or other suitable analgesic-antipyretic
• Warm or cold compresses for parotid pain
• Soft diet; avoid sour foods that increase salivation
• Scrotal support, rest, analgesia, and cold packs in orchitis

Prevention

• MMR vaccine is the main preventive measure.
• Two doses are used in routine immunization schedules.
• Isolate affected persons for 5 days after onset of parotitis.
• Avoid sharing utensils, cups, or saliva-contaminated items.

Exam points

• Cause: mumps virus, a paramyxovirus
• Transmission: droplets and saliva
• Hallmark: painful parotitis
• Major male complication: orchitis
• Major neurological complication: aseptic meningitis
• Prevention: MMR vaccine

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3. Rabies

Definition

Source and mode of transmission

Reservoirs

• Dogs are the major source of human rabies in many endemic countries.
• Other animals include cats, bats, foxes, jackals, wolves, and monkeys.

Transmission

• Bite of a rabid animal
• Scratch contaminated with saliva
• Lick over broken skin
• Saliva contact with mucous membranes
• Bat exposure

Pathogenesis

1. Virus is inoculated through a bite, scratch, or mucosa.
2. It replicates locally in muscle/connective tissue.
3. It enters peripheral nerves at neuromuscular junctions.
4. It travels centripetally by retrograde axonal transport to the spinal cord and brain.
5. It causes encephalitis.
6. It then spreads centrifugally to salivary glands and other tissues.

Incubation period

• Deep or multiple bites
• Bites on face, head, neck, hands, or fingers
• Heavy viral inoculum
• Young age

Clinical features

1. Prodromal stage

• Fever
• Malaise
• Headache
• Anxiety and irritability
• Nausea and vomiting
• Pain, tingling, burning, or itching at the bite site: highly suggestive feature

2. Acute neurologic stage

Furious rabies

• Hyperactivity and agitation
• Anxiety, confusion, hallucinations
• Hydrophobia: painful pharyngeal spasms on attempting to drink water
• Aerophobia: spasms triggered by air movement
• Hypersalivation
• Autonomic instability
• Alternating periods of agitation and lucidity

Paralytic rabies

• Ascending flaccid paralysis
• May resemble Guillain-Barre syndrome
• Hydrophobia is less prominent
• Progresses to coma and respiratory failure

3. Coma and death

• Coma
• Respiratory paralysis
• Cardiac arrhythmia
• Death usually occurs within days after neurologic symptoms begin

Diagnosis

• RT-PCR on saliva
• PCR or antigen detection in nuchal skin biopsy
• Rabies virus antibodies in serum and CSF
• Corneal impression smears in selected settings

Management of clinical rabies

• Intensive care
• Airway and ventilatory support
• Sedation and analgesia
• Management of autonomic instability
• Psychological support and palliative care when appropriate

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Post-exposure prophylaxis

Immediate wound management

1. Wash and flush the wound thoroughly with soap and running water for at least 15 minutes.
2. Apply a virucidal antiseptic such as povidone-iodine if available.
3. Avoid irritants, tight bandaging, and unnecessary suturing.
4. Give tetanus prophylaxis and antibiotics when clinically indicated.
5. Assess the exposure category and start vaccine promptly when indicated.

WHO exposure categories

Rabies immunoglobulin

• Infiltrate as much as possible into and around all wounds.
• Any remaining calculated volume may be administered away from the vaccine injection site, in line with local policy.
• It should be given as soon as possible with PEP. If unavailable initially, it may be administered within 7 days after the first vaccine dose.

Vaccine

• Start vaccination immediately for category II and III exposure.
• Previously vaccinated persons generally need wound care and abbreviated vaccine booster doses, but no immunoglobulin.
• Never inject rabies vaccine into the gluteal region.

Pre-exposure prophylaxis

• Veterinarians
• Animal handlers
• Laboratory workers handling rabies virus
• Wildlife workers
• Selected travellers or residents in highly endemic remote areas with limited access to PEP

Prevention

• Mass vaccination of dogs
• Control of stray dog populations through humane public-health measures
• Public education on immediate wound washing and urgent medical care after any animal bite
• Pre-exposure vaccination for high-risk groups
• Availability of vaccine and rabies immunoglobulin at treatment centres

Exam points

• Agent: rabies virus, genus Lyssavirus
• Shape: bullet-shaped RNA virus
• Common source in endemic regions: dog
• Cardinal symptoms: hydrophobia and aerophobia
• Once symptomatic: almost always fatal
• PEP: immediate wound washing + vaccine for category II/III + immunoglobulin for category III exposure# 1. Poliomyelitis

Definition

Causative agent

• Poliovirus, an enterovirus of the family Picornaviridae
• Three serotypes: poliovirus types 1, 2, and 3
• Wild poliovirus types 2 and 3 have been eradicated; type 1 remains the wild type of concern.

Transmission

• Mainly faeco-oral transmission
• Less commonly through oral-oral spread
• Virus multiplies in the pharynx and intestine and is shed in stool.
• Incubation period: usually 7-14 days, range about 3-35 days.

Pathogenesis

1. Virus enters through mouth.
2. Multiplies in pharynx and intestinal mucosa.
3. Produces viraemia.
4. In a small proportion, virus invades the CNS.
5. It selectively damages anterior horn cells of spinal cord and motor nuclei of brainstem.
6. This results in lower-motor-neuron paralysis.

Clinical forms

1. Inapparent infection

• Most infections are asymptomatic.
• The person may still shed virus and transmit infection.

2. Abortive poliomyelitis

• Mild fever
• Sore throat
• Malaise
• Headache
• Vomiting
• Recovery is complete without CNS involvement.

3. Non-paralytic poliomyelitis

• Aseptic meningitis
• Fever, headache, vomiting
• Neck stiffness
• Back and limb pain
• No paralysis

4. Paralytic poliomyelitis

Spinal poliomyelitis

• Acute, asymmetrical flaccid paralysis
• More common in lower limbs
• Reduced or absent reflexes
• Hypotonia
• No sensory loss
• Muscle wasting develops later

Bulbar poliomyelitis

• Involves cranial nerve nuclei and respiratory centres
• Dysphagia, nasal voice, weak cough
• Respiratory insufficiency
• May be fatal

Bulbospinal poliomyelitis

• Combined spinal and bulbar involvement

Diagnosis

• Clinical suspicion in any child with acute flaccid paralysis (AFP)
• Stool samples for poliovirus culture or RT-PCR
• Two stool samples, collected 24-48 hours apart and as early as possible after onset of paralysis, are used in surveillance.
• CSF may show findings of aseptic meningitis.

Treatment

• Bed rest during acute stage
• Analgesics and antipyretics
• Maintenance of airway and respiratory support when needed
• Management of swallowing difficulty
• Physiotherapy and passive range-of-motion exercises
• Prevention of contractures and deformities
• Orthoses, corrective surgery, and rehabilitation for residual paralysis

Prevention

Vaccines

• OPV: oral polio vaccine, live attenuated
• IPV: inactivated polio vaccine, injectable

Key exam points

• Agent: poliovirus, an enterovirus
• Spread: faeco-oral route
• Site of lesion: anterior horn cells
• Paralysis: asymmetric, flaccid, lower-motor-neuron type, without sensory loss
• Prevention: OPV/IPV and AFP surveillance

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2. Plague

Definition

Causative organism

• Yersinia pestis
• Gram-negative coccobacillus
• Shows bipolar staining, producing a “safety-pin” appearance with special stains.

Reservoir and vector

• Reservoir: wild rodents, such as rats, squirrels, and other small mammals
• Vector: rat flea, especially Xenopsylla cheopis
• Human infection may occur through:
  • Bite of an infected flea
  • Handling infected animals or tissues
  • Inhalation of droplets from a patient or animal with pneumonic plague

Incubation period

Types and clinical features

1. Bubonic plague

• Sudden high fever, chills, severe malaise
• Painful regional lymphadenitis called a bubo
• Bubo is usually inguinal, femoral, axillary, or cervical
• The node is enlarged, tender, and may suppurate
• A flea-bite lesion may be present

2. Septicaemic plague

• Severe sepsis and shock
• Disseminated intravascular coagulation
• Purpura, ecchymoses, and gangrene
• Acral necrosis may cause black discoloration, historically contributing to the term “Black Death”
• Multiorgan failure

3. Pneumonic plague

• Sudden fever and severe toxicity
• Cough, dyspnoea, chest pain
• Haemoptysis or bloody sputum
• Rapid progression to respiratory failure

Diagnosis

• Aspirate from bubo, blood, sputum, or CSF as relevant
• Gram stain or special stains may demonstrate bipolar staining bacilli
• Culture, antigen testing, PCR, or serology in specialist laboratories
• Inform the laboratory if plague is suspected because of biosafety requirements.

Treatment

• Gentamicin
• Streptomycin
• Ciprofloxacin or levofloxacin
• Doxycycline

Prevention and control

• Rodent control and environmental sanitation
• Flea control before rodent destruction
• Avoid handling sick or dead rodents and animals
• Protective measures for persons working with animals in endemic regions
• Droplet precautions for pneumonic plague
• Antibiotic post-exposure prophylaxis for close contacts of pneumonic plague, based on public-health guidance

Key exam points

• Agent: Yersinia pestis
• Vector: rat flea, Xenopsylla cheopis
• Classical lesion: painful bubo
• Most infectious form: pneumonic plague
• Diagnosis: bubo aspirate/culture/PCR
• Treatment: prompt aminoglycoside, fluoroquinolone, or doxycycline-based therapy

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3. Meningitis

Definition

Common causes

Acute bacterial meningitis

Other important types

• Viral meningitis: enteroviruses, mumps virus, herpes viruses
• Tuberculous meningitis: Mycobacterium tuberculosis
• Fungal meningitis: especially Cryptococcus in immunocompromised persons

Pathogenesis of bacterial meningitis

1. Organisms colonize nasopharynx or enter bloodstream from another site.
2. Bacteraemia allows crossing of the blood-brain barrier.
3. Organisms multiply in CSF.
4. Inflammatory cytokines increase permeability of blood-brain barrier.
5. Cerebral oedema, raised intracranial pressure, vasculitis, and impaired cerebral perfusion occur.
6. Untreated disease may rapidly cause coma, shock, and death.

Clinical features

Classical triad

Fever + headache + neck stiffness

• Vomiting
• Photophobia
• Altered sensorium, confusion, or coma
• Seizures
• Irritability or poor feeding in infants
• Positive Kernig or Brudzinski signs
• Focal neurological deficit in complicated disease

Meningococcal meningitis

• Petechial or purpuric rash
• Septicaemia
• Shock
• Disseminated intravascular coagulation
• Waterhouse-Friderichsen syndrome

Diagnosis

Initial investigations

• Blood culture before antibiotics, if this does not delay treatment
• Complete blood count, blood glucose, renal and liver function tests
• Lumbar puncture and CSF examination, if safe
• CSF Gram stain, culture, and PCR where available

When to do CT before lumbar puncture

• Focal neurological deficit
• Papilloedema
• New-onset seizure
• Markedly impaired consciousness
• Known CNS disease
• Severe immunocompromise

CSF findings

Treatment of suspected acute bacterial meningitis

General principles

• Admit urgently.
• Start empiric IV antibiotics immediately.
• Give dexamethasone before or with the first antibiotic dose when appropriate, particularly when pneumococcal meningitis is suspected.
• Treat seizures, shock, hypoxia, and raised intracranial pressure.
• Modify therapy after culture and sensitivity results.

Common empiric approach in adults

• Third-generation cephalosporin, such as ceftriaxone or cefotaxime, plus vancomycin
• Add ampicillin/amoxicillin when Listeria risk is present, for example older age, pregnancy, significant immunosuppression, or certain comorbidities.

Prevention

Vaccination

• Hib vaccine
• Pneumococcal conjugate vaccine
• Meningococcal vaccines

Chemoprophylaxis for meningococcal contacts

Infection control

• Droplet precautions for suspected or confirmed meningococcal meningitis.
• Continue until effective antibiotics have been given for at least 24 hours.

Key exam points

• Meningitis: inflammation of meninges
• Classic triad: fever, headache, neck stiffness
• Most important emergency form: acute bacterial meningitis
• CSF in bacterial meningitis: neutrophils, high protein, low glucose
• Do not delay IV antibiotics for lumbar puncture or CT in a seriously ill patient
• Prevention: Hib, pneumococcal, and meningococcal vaccination# 1. Encephalitis

Definition

Causes

Infectious causes

Non-infectious causes

• Autoimmune encephalitis, such as anti-NMDA receptor encephalitis
• Post-infectious encephalomyelitis, for example acute disseminated encephalomyelitis (ADEM)

Pathogenesis

• The organism enters the central nervous system through blood, peripheral nerves, or direct extension.
• Viral replication and host inflammatory response cause cerebral oedema, neuronal injury, haemorrhage, raised intracranial pressure, seizures, and focal deficits.
• HSV classically involves the temporal and frontal lobes.

Clinical features

General manifestations

• Fever and headache
• Altered behaviour, irritability, confusion, delirium, or reduced consciousness
• Seizures
• Nausea and vomiting
• Photophobia
• Neck stiffness may be present if there is associated meningitis

Focal signs

• Aphasia
• Memory disturbance
• Hemiparesis
• Cranial nerve palsies
• Ataxia
• Movement disorders

Features suggesting HSV encephalitis

• Fever with altered mental status
• Personality or behavioural change
• Focal seizures, especially temporal-lobe seizures
• Aphasia or memory impairment
• MRI abnormalities in temporal lobes

Diagnosis

Investigations

• Blood culture, complete blood count, glucose, electrolytes, renal and liver function tests
• Neuroimaging, preferably MRI brain
• Lumbar puncture, if safe
• CSF examination:
  • Cells, protein, glucose
  • Gram stain and bacterial culture
  • HSV PCR and other pathogen-specific PCR tests
• EEG, especially with seizures or suspected temporal-lobe involvement

CSF findings in viral encephalitis

• Lymphocytic pleocytosis
• Mild to moderate protein rise
• Usually normal glucose
• HSV encephalitis may show red blood cells due to haemorrhagic necrosis

Treatment

Immediate management

1. Admit urgently.
2. Stabilize airway, breathing, and circulation.
3. Manage seizures.
4. Control fever and maintain fluids/electrolytes.
5. Monitor for raised intracranial pressure.
6. Start empiric treatment without waiting for confirmation when HSV encephalitis is suspected.

Specific treatment

• IV acyclovir should be started promptly in suspected HSV or VZV encephalitis.
• Appropriate antibiotics are added if bacterial meningitis or meningoencephalitis cannot be excluded.
• Treat tuberculosis, malaria, autoimmune encephalitis, or other identified causes specifically.

Complications

• Persistent epilepsy
• Memory loss and cognitive impairment
• Personality changes
• Motor deficits
• Hearing or visual impairment
• Coma and death

Prevention

• Vaccination against measles, mumps, rubella, varicella, Japanese encephalitis, and rabies where indicated
• Mosquito control and personal protection against mosquito bites
• Early recognition and treatment of infections

Key exam points

• Encephalitis = inflammation of brain tissue.
• Cardinal sign: altered mental status.
• Important treatable cause: HSV encephalitis.
• Diagnosis: MRI brain plus CSF PCR.
• Immediate treatment: IV acyclovir if HSV is suspected.

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2. Chikungunya Fever

Definition

Vector and transmission

• Vector: female Aedes aegypti and Aedes albopictus
• These mosquitoes are mainly day-biting.
• They breed in clean stagnant water in containers, coolers, tyres, flower pots, and tanks.
• Humans are the main amplifying host during outbreaks.
• Incubation period: usually 3-7 days, range 1-12 days.

Clinical features

Acute phase

• Sudden onset high fever
• Severe, symmetrical polyarthralgia or polyarthritis
• Joint swelling and stiffness
• Headache
• Myalgia
• Fatigue
• Maculopapular rash
• Nausea and vomiting
• Conjunctival injection or photophobia in some patients

• Wrists
• Ankles
• Small joints of hands and feet
• Knees
• Elbows

Rash

• Usually maculopapular
• Appears 2-5 days after onset of fever
• May involve trunk, limbs, face, palms, and soles
• Pruritus may occur

Chronic chikungunya arthritis

• Chronic inflammatory polyarthritis
• Morning stiffness
• Tendinitis or tenosynovitis
• Functional limitation
• May mimic rheumatoid arthritis

Complications

• Severe dehydration
• Myocarditis
• Hepatitis
• Uveitis
• Acute kidney injury
• Encephalitis, meningoencephalitis, seizures
• Guillain-Barre syndrome
• Neonatal chikungunya, especially with maternal infection near delivery

Differential diagnosis

• Dengue fever
• Zika virus infection
• Malaria
• Leptospirosis
• Enteric fever
• Acute viral arthritis
• Rheumatoid arthritis

Chikungunya versus dengue

Diagnosis

First week of illness

• RT-PCR for chikungunya viral RNA
• Viral isolation in specialist laboratories

After first week

• Chikungunya-specific IgM antibody test
• Rising IgG titres in paired sera can support diagnosis

Routine tests

• Complete blood count
• Liver and renal function tests when severe illness is suspected
• Test for dengue and malaria where epidemiologically relevant

Treatment

Acute management

• Rest
• Adequate oral fluids
• Paracetamol for fever and pain
• Cold compresses for painful joints
• Monitor vulnerable patients for complications

After dengue has been excluded

• NSAIDs may be used for persistent joint pain if clinically appropriate.
• Persistent arthritis may require physiotherapy, rehabilitation, rheumatology evaluation, and selected anti-inflammatory or disease-modifying treatment under specialist care.

Prevention and control

• Eliminate stagnant water and mosquito breeding containers.
• Cover water storage vessels.
• Use repellents, full-sleeved clothing, screens, and nets.
• Community-based Aedes control is essential.
• Patients should avoid mosquito bites during the first week of illness to reduce onward transmission.

Key exam points

• Agent: chikungunya virus, an alphavirus.
• Vector: Aedes aegypti and Aedes albopictus.
• Hallmark: abrupt fever with severe symmetrical polyarthralgia.
• Chronic complication: persistent inflammatory arthritis.
• Diagnosis: RT-PCR early, IgM later.
• Treatment: supportive; use paracetamol first and exclude dengue before NSAIDs.

HIV/AIDS: Detailed Exam Note

Definition

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Causative agent

• HIV belongs to the family Retroviridae, subfamily Lentivirinae.
• It is an enveloped, single-stranded RNA retrovirus.
• Two main types:
  • HIV-1: common worldwide and more virulent.
  • HIV-2: mainly found in West Africa; less transmissible and progresses more slowly.

Structure of HIV

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Modes of transmission

Major routes

1. Sexual transmission
   • Vaginal or anal intercourse without effective barrier protection
   • Risk increases with other sexually transmitted infections, especially genital ulcers.
2. Blood-borne transmission
   • Transfusion of infected blood or blood products
   • Sharing contaminated needles or syringes
   • Unsafe injections
   • Organ transplantation from an infected donor
   • Occupational needle-stick injury
3. Mother-to-child transmission
   • During pregnancy
   • During labour and delivery
   • Through breastfeeding

HIV is not transmitted by

• Handshakes, hugging, sharing food, utensils, toilets, or clothes
• Mosquitoes or other insects
• Saliva, tears, sweat, or casual contact
• Coughing or sneezing

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Pathogenesis

1. HIV enters the body and binds to the CD4 receptor on T-helper lymphocytes, macrophages, and dendritic cells.
2. Viral gp120 also binds a co-receptor:
   • CCR5, commonly in early infection
   • CXCR4, commonly in later infection
3. Viral RNA is converted to DNA by reverse transcriptase.
4. Viral DNA enters the host nucleus and is integrated into host DNA by integrase.
5. New viral particles are produced and released.
6. Ongoing viral replication and immune activation progressively reduce CD4+ T-cell number and function.
7. Severe CD4 depletion causes opportunistic infections and malignancies.

Consequences of CD4 depletion

• Reduced cell-mediated immunity
• Reduced macrophage activation
• Defective delayed hypersensitivity responses
• Increased risk of tuberculosis, Pneumocystis pneumonia, candidiasis, toxoplasmosis, cryptococcosis, and other opportunistic diseases

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Natural history of untreated HIV infection

1. Acute HIV infection

• Fever
• Sore throat
• Rash
• Generalized lymphadenopathy
• Myalgia
• Headache
• Oral ulcers
• Diarrhoea
• Aseptic meningitis in some patients

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2. Clinical latency or chronic HIV infection

• May last for years without antiretroviral therapy.
• The patient may be asymptomatic.
• Persistent generalized lymphadenopathy may occur.
• Viral replication and CD4-cell loss continue despite apparent clinical wellness.

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3. Symptomatic HIV disease

• Unexplained weight loss
• Persistent fever
• Chronic diarrhoea
• Persistent generalized lymphadenopathy
• Recurrent bacterial infections
• Oral candidiasis
• Herpes zoster
• Recurrent respiratory infections
• Tuberculosis

---

4. AIDS

• A CD4 count below 200 cells/mm³, or
• An AIDS-defining opportunistic infection or malignancy, regardless of CD4 count.

---

Clinical manifestations

Constitutional manifestations

• Fever
• Night sweats
• Weight loss
• Fatigue
• Chronic diarrhoea
• Persistent lymphadenopathy

Dermatological manifestations

• Seborrhoeic dermatitis
• Oral candidiasis
• Herpes zoster
• Recurrent herpes simplex infection
• Molluscum contagiosum
• Pruritic papular eruption
• Kaposi sarcoma
• Bacillary angiomatosis

Oral manifestations

• Oral candidiasis
• Oral hairy leukoplakia
• Recurrent aphthous ulcers
• Periodontal disease
• Recurrent herpes labialis

Respiratory manifestations

• Recurrent bacterial pneumonia
• Tuberculosis
• Pneumocystis jirovecii pneumonia
• Pulmonary cryptococcosis
• Cytomegalovirus pneumonitis, rarely

Gastrointestinal manifestations

• Chronic diarrhoea
• Oesophageal candidiasis
• Cryptosporidiosis
• Isosporiasis
• Cytomegalovirus colitis
• Tuberculosis
• Non-Hodgkin lymphoma

Neurological manifestations

• HIV-associated neurocognitive disorder
• Cryptococcal meningitis
• Toxoplasma encephalitis
• Tuberculous meningitis
• Progressive multifocal leukoencephalopathy
• CMV retinitis with visual loss
• Peripheral neuropathy

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Opportunistic infections according to CD4 count

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AIDS-defining conditions

• Pneumocystis jirovecii pneumonia
• Oesophageal candidiasis
• Cryptococcosis outside the lungs
• Toxoplasmosis of brain
• Cytomegalovirus retinitis
• Chronic cryptosporidiosis
• Recurrent bacterial pneumonia
• Recurrent salmonella septicaemia
• Tuberculosis in many clinical staging systems
• Disseminated histoplasmosis
• Kaposi sarcoma
• Invasive cervical carcinoma
• Non-Hodgkin lymphoma
• Primary CNS lymphoma
• HIV wasting syndrome

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Diagnosis of HIV

1. Screening tests

• HIV-1 and HIV-2 antibodies
• p24 antigen

2. Confirmatory tests

3. Nucleic acid testing

• Suspected acute HIV infection
• Infants born to mothers with HIV
• Indeterminate serology
• Monitoring viral load

4. Baseline assessment after diagnosis

• CD4 count
• HIV viral load
• Complete blood count
• Renal and liver function tests
• Hepatitis B and C screening
• Syphilis and other STI testing
• Tuberculosis screening
• Pregnancy test where relevant
• Evaluation for opportunistic infections
• Resistance testing where available

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Treatment: Antiretroviral therapy

Principles

• All persons diagnosed with HIV should start ART as soon as possible, regardless of CD4 count.
• ART suppresses viral replication, raises CD4 count, prevents opportunistic disease, improves survival, and prevents sexual transmission when viral suppression is sustained.
• Current ART is highly effective but is not curative because HIV forms a persistent latent reservoir. [Goldman-Cecil Medicine, p. 3584]

Standard first-line ART

Tenofovir + Lamivudine + Dolutegravir
Often abbreviated as TLD

• Tenofovir: nucleoside/nucleotide reverse transcriptase inhibitor
• Lamivudine: nucleoside reverse transcriptase inhibitor
• Dolutegravir: integrase strand-transfer inhibitor

Major antiretroviral drug classes

Monitoring ART

• Adherence assessment at every visit
• Viral load monitoring is the main measure of treatment response
• CD4 monitoring, especially at baseline and in advanced disease
• Monitoring for drug toxicity and interactions
• Evaluation for treatment failure and resistance if viral load remains elevated

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Undetectable = Untransmittable

U = U: Undetectable = Untransmittable

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Treatment of opportunistic infections

Principles

• Diagnose and treat the opportunistic infection promptly.
• Start or optimize ART, with timing tailored to the particular infection.
• Check for drug interactions, especially with rifampicin-containing tuberculosis treatment.
• Prevent recurrence using prophylaxis when indicated.
• Watch for immune reconstitution inflammatory syndrome (IRIS).

IRIS

• Tuberculosis
• Cryptococcosis
• Cytomegalovirus
• Herpes zoster

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Opportunistic infection prophylaxis

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HIV and tuberculosis

Importance

• HIV increases risk of both primary tuberculosis and reactivation of latent TB.
• TB may present atypically in advanced HIV, including extrapulmonary or disseminated disease.
• All persons with HIV should be screened regularly for TB symptoms.

Management principles

• Treat active TB promptly.
• Start ART during TB treatment, with the timing determined by CD4 count and clinical status.
• Give cotrimoxazole prophylaxis where indicated.
• Consider TB preventive treatment after active TB is excluded.
• Check interactions between rifampicin and ART.

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Prevention of HIV

1. Safe sexual practices

• Correct and consistent condom use
• Testing and treatment for STIs
• Limiting sexual exposure risk
• Partner testing and counselling
• ART with viral suppression for people living with HIV

2. Pre-exposure prophylaxis

• Partners of persons with untreated or unsuppressed HIV
• Persons with recurrent high-risk sexual exposure
• People who inject drugs and share injecting equipment
• Other populations at substantial risk, according to local guidelines

3. Post-exposure prophylaxis

• Start as soon as possible, ideally within hours.
• It should generally be started within 72 hours of exposure.
• A complete course is required under medical guidance.

4. Prevention of mother-to-child transmission

• Routine HIV testing in pregnancy
• Immediate lifelong ART for the pregnant person with HIV
• Viral load monitoring
• Safe delivery planning
• Appropriate infant antiretroviral prophylaxis and HIV testing
• Infant-feeding advice according to local guidelines and availability of safe replacement feeding

5. Blood and injection safety

• Screening of donated blood
• Sterile needles and syringes
• Safe injection practices
• Standard precautions in healthcare settings
• Avoid sharing needles, razors, or other blood-contaminated instruments

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HIV vaccine

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Counselling and psychosocial care

• Confidentiality and non-discrimination
• Adherence counselling
• Partner notification and testing support
• Family-planning and reproductive counselling
• Nutritional assessment
• Screening for depression, substance use, and violence
• Social support and stigma reduction

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Short exam summary

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Quick Differentiation Points for Exams

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High-yield Differentiation Mnemonics

Dengue vs Chikungunya

“Dengue BLEEDS, Chikungunya BENDS.”

Measles vs Chickenpox

“Measles MARCHES, Chickenpox MIXES.”

• Measles marches from face to trunk to limbs, with lesions of the same stage.
• Chickenpox mixes lesions at multiple stages, macules, papules, vesicles, and crusts, at the same time.

Meningitis vs Encephalitis

“MENINGitis = MENINGES, ENCEPHalitis = ENCEPHALON.”

• Meningitis: fever, headache, neck stiffness, photophobia.
• Encephalitis: fever plus altered consciousness, behavioural change, seizures, or focal neurological deficit.

Polio vs Guillain-Barre syndrome

“POLIO is Patchy; GBS goes Gradually Both Sides.”

• Polio: asymmetric flaccid paralysis, no sensory loss.
• Guillain-Barre syndrome: usually symmetrical ascending weakness, often with sensory symptoms.

Kala-azar vs Malaria

“Kala-azar = Huge spleen + Low all cell lines.”

• Kala-azar: prolonged fever, massive splenomegaly, pancytopenia.
• Malaria: intermittent fever with chills/rigors; malaria parasites detectable in blood.

Rabies vs Tetanus

“Rabies fears water; tetanus locks the jaw.”

• Rabies: hydrophobia, aerophobia, agitation after animal exposure.
• Tetanus: trismus, muscle rigidity, painful spasms, but no hydrophobia.

Filariasis vs Kala-azar

“Filaria blocks lymph; kala-azar fills spleen.”

• Filariasis: lymphoedema, elephantiasis, hydrocele.
• Kala-azar: fever, weight loss, massive spleen, pancytopenia.

HIV/AIDS

“HIV lowers CD4, infections open the door.”

• <200: Pneumocystis jirovecii pneumonia
• <100: Toxoplasmosis, cryptococcosis
• <50: CMV retinitis, disseminated MAC

“200 PJP, 100 Toxo, 50 CMV.”

Infectious Disease Mnemonics One Page

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Myopathies are a broad examination topic. A complete note is best divided into:

1. Approach to myopathy: clinical pattern, differential diagnosis, investigations, and general management
2. Muscular dystrophies: Duchenne, Becker, myotonic dystrophy, limb-girdle dystrophies, facioscapulohumeral dystrophy
3. Inflammatory myopathies: polymyositis, dermatomyositis, immune-mediated necrotizing myopathy, inclusion-body myositis
4. Metabolic, endocrine, drug-induced and toxic myopathies
5. Periodic paralysis, mitochondrial myopathies, and congenital myopathies

1. Approach and classification of myopathies
2. Muscular dystrophies
3. Inflammatory myopathies
4. Metabolic, endocrine, and toxic myopathies
5. All sections as a concise revision note