mumps 2nd yr mbbs microbiology refer apurba sastri cover definiTION DIAGRAM OF VIRUS clinical manifestation virulence factor,pathogenesis symptoms suppurative complications, non suppurative complications, lab diagnosis treatment answer in details

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I now have all the content needed. Let me compile the full detailed answer in the style of Apurba Sastri's MBBS microbiology approach.

MUMPS - Complete MBBS 2nd Year Microbiology Notes

(Based on standard microbiology textbooks aligned with Apurba Sastri's 2nd year syllabus)

1. DEFINITION

Mumps is an acute, self-limited, systemic viral illness caused by the mumps virus (a paramyxovirus), classically characterized by fever and non-suppurative parotitis (painful swelling of the parotid salivary glands). It can also involve other organs via viremia - testes, ovaries, pancreas, meninges, and CNS.
  • Sherris & Ryan's Medical Microbiology, 8th ed.: "Mumps is transmitted through respiratory tract and replicates in respiratory tract epithelium and local lymph nodes followed by fever and swelling of parotid glands (parotitis) unilateral or bilateral."

2. DIAGRAM OF THE VIRUS

The mumps virus is a paramyxovirus - an enveloped, helical, negative-sense single-stranded RNA virus.
Mumps virus structure diagram
Key structural components:
ComponentDescription
GenomeSingle-stranded, negative-sense RNA, ~15.3 kb
CapsidHelical nucleocapsid
EnvelopeLipid bilayer (derived from host cell membrane)
HN spikeHemagglutinin-Neuraminidase glycoprotein - mediates attachment to sialic acid on host cells AND neuraminidase activity
F spikeFusion protein - mediates fusion of viral envelope with host cell plasma membrane
Matrix (M) proteinLines the inner surface of the envelope
Small hydrophobic (SH) proteinHypervariable - used for genotyping
Replication: Occurs in the cytoplasm using its own viral RNA-dependent RNA polymerase. Progeny viruses are released by budding from plasma membranes.
Only one serotype is known; 12 genotypes exist (A-N, excluding E and M).

3. VIRULENCE FACTORS

Virulence FactorFunction
HN (Hemagglutinin-Neuraminidase)Attaches to sialic acid receptors on host epithelial cells; neuraminidase activity helps in release of new virions; mediates agglutination of RBCs
F (Fusion) proteinFuses viral envelope with host cell membrane, allowing entry of nucleocapsid into cytoplasm; promotes syncytia/giant cell formation
Lipid envelopeProtects the virus from host immune detection; facilitates cell-to-cell spread
Tropism for glandular and neural tissueVirus has wide tissue tropism - salivary glands, testes, ovaries, pancreas, CNS; direct cytopathic and immune-mediated damage
Ability to infect mononuclear cellsFacilitates viremia and spread to distant organs
The virus is rapidly inactivated by formalin, ether, chloroform, heat, and UV light - important for vaccine preparation.

4. PATHOGENESIS

Mumps parotitis - clinical photo
Mumps parotitis - characteristic swelling below the earlobe (Sherris & Ryan)
Step-by-step pathogenesis:
Inhalation of respiratory droplets / direct contact with saliva
              ↓
Primary replication in NASAL MUCOSA / UPPER RESPIRATORY EPITHELIUM
              ↓
Spread to REGIONAL LYMPH NODES
(Mononuclear cells infected → viremia develops)
              ↓
PRIMARY VIREMIA (lasts 3-5 days)
              ↓
Dissemination to multiple organs:
    → SALIVARY GLANDS → PAROTITIS (most common)
    → TESTES → ORCHITIS
    → OVARIES → OOPHORITIS
    → PANCREAS → PANCREATITIS
    → CNS (via choroid plexus or infected mononuclear cells) → MENINGITIS / ENCEPHALITIS
    → KIDNEY → VIRURIA (common)
    → COCHLEA → SENSORINEURAL HEARING LOSS
              ↓
TISSUE DAMAGE: perivascular and interstitial mononuclear cell infiltrates,
hemorrhage, edema, necrosis of acinar and ductal epithelial cells
              ↓
IMMUNE RESPONSE: Humoral (IgM early, IgG lifelong) + Cell-mediated immunity
Pathological findings:
  • Salivary glands: edema, mononuclear cell infiltration, necrosis of acinar and ductal cells; elevated serum/urine amylase
  • Testes: necrosis of germinal epithelium of seminiferous tubules
  • CNS encephalitis: often para- or post-infectious - perivenous demyelination + perivascular mononuclear cell inflammation (not always direct cytotoxic viral invasion)
  • Humans are the only known natural reservoir

5. CLINICAL MANIFESTATIONS

Incubation Period

  • Range: 12-25 days
  • Average: 16-18 days
  • Infectious period: 2 days BEFORE to 5 days AFTER onset of parotitis

Prodromal Stage (1-2 days before parotitis):

  • Low-grade fever
  • Malaise
  • Myalgia (muscle aches)
  • Headache
  • Anorexia

Main Phase - Parotitis:

Parotid gland anatomy diagram
Anatomy of the parotid gland - ear-gland axis between the earlobe and angle of mandible
  • Parotid swelling - bilateral in most cases (~2/3); unilateral in ~1/3 of cases
  • Swelling obliterates the space between the earlobe and the angle of the mandible (ear-gland axis)
  • Accompanied by tenderness
  • The orifice of the parotid duct (Stensen's duct) is red and swollen - an important clinical sign
  • Earache and jaw pain; difficulty eating, swallowing, or talking
  • Dysarthria (from trismus and inflammation)
  • Lasts 5-7 days, total resolution within 10 days
  • ~20% of infections are asymptomatic
  • Submaxillary and sublingual glands may also be involved (less commonly)
Note: ~20% of unvaccinated patients have asymptomatic infection but can still transmit disease.

6. SUPPURATIVE COMPLICATIONS

Mumps itself causes non-suppurative parotitis (no pus formation). However, the following suppurative (bacterial secondary) complications can occasionally occur:
ComplicationFeatures
Secondary bacterial parotitisBacterial superinfection (Staphylococcus aureus, Streptococcus) of the inflamed parotid gland; pus may be expressed from Stensen's duct; requires antibiotics
Bacterial meningitisRare; secondary bacterial infection complicating mumps-induced meningeal inflammation
Bacterial orchitis/epididymo-orchitisRare bacterial superinfection on top of viral orchitis
In Apurba Sastri's classification, suppurative complications = secondary bacterial infections of inflamed tissues; mumps virus itself produces non-suppurative pathology.

7. NON-SUPPURATIVE COMPLICATIONS

These are the primary viral complications - direct or immune-mediated damage by the mumps virus itself. These are far more common and clinically significant.

A. GENITOURINARY Complications

ComplicationFrequencyFeatures
Orchitis10-30% of unvaccinated post-pubertal malesMost common complication; fever + painful testicular swelling; usually 1st week of parotitis but can appear up to 6 weeks later; bilateral in 10-30% of cases; pain and swelling last ~1 week; testicular atrophy in 30-50% of affected testes; sterility is rare
Oophoritis~7% unvaccinated post-pubertal femalesLower abdominal pain, vomiting; usually benign
MastitisUp to 30% unvaccinated post-pubertal womenBreast swelling and tenderness

B. GASTROINTESTINAL Complications

ComplicationFrequencyFeatures
Pancreatitis~4% unvaccinated patientsUpper abdominal pain, nausea, vomiting; elevated serum amylase AND lipase (amylase alone is also elevated in parotitis - lipase elevation helps distinguish pancreatitis); usually self-limited

C. CNS Complications

ComplicationFrequencyFeatures
Aseptic meningitisUp to 10% unvaccinated; ≤1% vaccinatedMost common CNS complication; CSF pleocytosis (subclinical CNS involvement up to 55%); stiff neck, headache, drowsiness ~5 days after parotitis; self-limited; parotitis may be absent in 1/3 of cases
Encephalitis<1%High fever, marked change in consciousness, seizures, focal neurologic signs; EEG abnormalities; mortality ~1.5%; permanent sequelae possible
Sensorineural hearing lossUp to 4% unvaccinatedUsually sudden onset, unilateral, transient; rare bilateral/permanent
Transverse myelitisRareSpinal cord involvement
Cerebellar ataxiaRare
Facial palsyRare
Guillain-Barré syndromeRare
HydrocephalusRare

D. CARDIAC Complications

  • Myocarditis - rare but severe; ECG abnormalities reported in up to 15% of mumps cases
  • Endocardial fibroelastosis - rare

E. OTHER Non-suppurative Complications

  • Thyroiditis
  • Nephritis (abnormal renal function common, but severe nephritis rare)
  • Arthritis
  • Hepatic involvement
  • Keratouveitis
  • Thrombocytopenic purpura
  • Pneumonia

8. LABORATORY DIAGNOSIS

A. Specimen Collection

  • Buccal swab (best specimen - parotid gland massaged for 30 seconds before collection)
  • Saliva / pharyngeal swab
  • Urine (virus present up to 14 days after parotitis onset)
  • CSF (if meningitis suspected)
  • Blood
Specimens should be collected within 5 days of parotitis onset for maximum yield (peak viral shedding); urine yield improves up to 10 days.

B. Virological Methods (Confirmatory)

TestDetails
RT-PCR (Gold Standard for diagnosis)Reverse transcription-PCR; most sensitive, specific, and rapid; detects viral RNA; preferred method especially in vaccinated patients
Virus cultureGold standard for isolation; grows in primary monkey kidney cell cultures or Vero cells; forms syncytial giant cells and produces viral hemagglutinin (hemadsorption); takes days-weeks

C. Serological Methods

TestDetails
ELISA / EIADetects mumps-specific IgM (early, within 5 days of onset) and IgG; most widely used
IgM detectionPresent within 5 days of onset; diagnosis of acute infection; may be negative in vaccinated persons (limitation)
IgG (paired sera)4-fold rise between acute and convalescent phase (2-3 weeks apart) = confirmation
Indirect Immunofluorescence (IF)Detects IgM and IgG
Complement fixation (CF)Uses S (soluble/nucleocapsid) and V (viral/envelope) antigens; anti-S antibodies rise early, anti-V antibodies persist longer
Hemagglutination inhibition (HI)Detects antibodies against HN protein
Neutralization testMost sensitive for immunity; not routinely used
Important caveat: In vaccinated patients, IgM may be absent or undetectable even with genuine infection. A positive IgG alone does not distinguish acute infection from prior vaccination.

D. Other Supportive Tests

  • Elevated serum/urine amylase - in parotitis and pancreatitis
  • Elevated serum lipase - specific for pancreatitis (not parotitis)
  • CSF analysis - lymphocytic pleocytosis, normal glucose, mildly elevated protein in aseptic meningitis

9. TREATMENT

There is NO specific antiviral treatment for mumps. Management is entirely supportive and symptomatic.
MeasureDetails
RestBed rest during febrile period
Analgesics/AntipyreticsParacetamol (acetaminophen) or NSAIDs for fever, pain, and malaise
Adequate hydrationOral fluids; IV fluids if vomiting severely (pancreatitis)
Soft dietAvoid acidic/spicy foods that stimulate salivation and worsen pain
Scrotal supportIce packs and scrotal support for orchitis to reduce pain and swelling
CorticosteroidsSometimes used for severe orchitis or encephalitis (no definitive RCT evidence)
IsolationDroplet precautions; isolate for 5 days from onset of parotitis

Prevention (Most Important!)

VaccineDetails
MMR vaccineLive attenuated mumps vaccine (Jeryl Lynn strain - genotype A) combined with measles + rubella
MMRVAlso includes varicella (chickenpox)
Schedule1st dose: 12-15 months of age; 2nd dose: 4-6 years of age
Seroconversion~80% after 1 dose; ~90% after 2 doses
Efficacy>99% reduction in cases with 2-dose schedule
3rd doseRecommended during outbreaks for high-risk individuals
ContraindicationsPregnancy, severe immunodeficiency, anaphylaxis to neomycin
Key point: MMR vaccine given after exposure does NOT prevent disease and is NOT recommended as post-exposure prophylaxis.

QUICK SUMMARY TABLE

FeatureDetails
Causative agentMumps virus - Paramyxoviridae family, Rubulavirus genus
GenomeSingle-stranded, negative-sense RNA
EnvelopeYes (HN and F spikes)
SerotypesOnly ONE serotype
ReservoirHumans only
TransmissionRespiratory droplets; direct contact with saliva
Incubation period12-25 days (average 16-18 days)
Infectious period2 days before to 5 days after parotitis onset
HallmarkNon-suppurative bilateral parotitis
Most common complicationOrchitis (in post-pubertal males)
DiagnosisRT-PCR (preferred) + ELISA IgM/IgG
TreatmentSupportive (no specific antiviral)
PreventionMMR vaccine (2 doses)
Sterility in orchitisRare despite testicular atrophy

Sources: Sherris & Ryan's Medical Microbiology 8th ed. | Harrison's Principles of Internal Medicine 22nd ed. (2025) | Jawetz, Melnick & Adelberg's Medical Microbiology 28th ed.
Note: Apurba Sastri's "Review of Microbiology and Immunology" was not available in the textbook library. This answer is compiled from equivalent-level standard microbiology and clinical medicine textbooks covering the same 2nd year MBBS syllabus content. The information matches the coverage style and depth of Apurba Sastri's text.
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