COMMON CHILDHOOD INFECTIONS

•	Viral fever.
•	Kawasaki disease.
•	Henoch Scholein purura.

Viral fevers in children

1.	Introduction

a.	Refers to undifferentiated febrile illnesses.

b.	Can be caused by many different viruses which are difficult to identify.

c.	Treatment consists of keeping the child comfortable and ensuring adequate hydration.

d.	Reassurance regarding self-limiting nature of illness and minimal risk of brain damage.

2.	Clinical features

a.	Fever can reach up to 41C.

b.	Child can be irritable when febrile, but usually better when afebrile.

c.	Constitutional symptoms:

i.	loss of appetite.

ii.	lethargy.

iii.	rhinorrhoea.

iv.	pharyngitis.

v.	muscle ache.

vi.	joint pains.

vii.	nausea.

viii.	loose stools. 

d.	Non-specific exanthem, usually maculopapular rash.

3.	Danger signs

a.	Extreme lethargy.

b.	Confusion.

c.	Markedly reduced urine output.

d.	Seizure.

e.	Severe headache.

Hand, Foot, Mouth Disease

1.	Background

a.	Caused by the enteroviruses.

b.	Most commonly coxsackie A16 and enterovirus 71.

c.	Transmission by fecal-oral route.

d.	More severe disease in younger children.

e.	Causes outbreaks among young children.

2.	Clinical features

a.	Asymptomatic or undifferentiated febrile illness.

b.	Short incubation period of 2 to 6 days.

c.	Oral lesions:

i.	ulcers on tongue and buccal mucosa.

ii.	results in food refusal because of tender lesions.

d.	Hand and feet lesions:

i.	vesicular and tender.

ii.	both dorsal and ventral surfaces.

3.	Complications

a.	Myocarditis and pericarditis.

b.	Aseptic meningitis.

4.	Diagnosis:

a.	Clinical.

b.	Isolation of virus from secretions and stools.

5.	Treatment

a.	Symptomatic by controlling fever and ensuring hydration.

b.	Isolation of infective person.

Varicella

1.	Background

a.	Caused by the varicella-zoster virus (VZV), HSV-3.

b.	Often a mild illness in children, but can cause significant morbidity and mortality, especially in adults.

c.	Highly contagious, spread from respiratory secretions or from vesicles.

2.	Clinical features

a.	Incubation period of 10 to 21 days.

b.	Prodrome of fever, malaise, headache, anorexia and rhinorrhoea.

c.	Rash:

i.	starts as pruritic, erythematous macules.

ii.	evolves to clear, fluid-filled vesicles.

iii.	polymorphic rash: lesions at different stages of evolution.

iv.	vesicular lesions in mucous membranes: oropharynx, conjunctivae, vagina.

3.	Severe progressive varicella

a.	Feared complication of primary varicella infection.

b.	Results in visceral organ involvement, DIC, haemorrhage.

c.	Severe abdominal pain and haemorrhagic vesicles are commonly seen.

d.	Risk highest in immunosuppressed patients.

4.	Complications

a.	Varicella pneumonia in adults which may be fatal.

b.	Varicella encephalitis: a cerebellar ataxia which resolves completely over days to weeks.

5.	Neonatal varicella

a.	Risk in babies whose mother develop varicella 1 week before or after delivery.

b.	Babies may develop a severe, disseminated form of varicella.

c.	Babies born 5 days before and up to 2 days after mum gets disease should receive varicella immunoglobulin (VZIG).

d.	Neonates with significant clinical disease should be treated with IV acyclovir.

6.	Diagnosis

a.	Clinical.

b.	PCR identification of viral DNA.

c.	Serological evidence of 4-fold rise in varicella specific IgG.

7.	Treatment

a.	Acyclovir.

b.	Immunization

Herpes Zoster

1.	Background

a.	A reactivation of latent varicella virus infection, the virus persisting in the dorsal root ganglia after primary infection.

b.	Lifetime risk is 10% in someone with a history of varicella.

c.	Occurs at all ages, the frequency increases with advancing age.

2.	Clinical features

a.	Groups of vesicles on an erythematous base sited over the distribution of the infected spinal or cranial sensory nerve (dermatome).

b.	Unilateral with a sharp central demarcation and usually involves thoracic or lumbar dermatomes or cranial nerves.

c.	Lesions associated with pain, hyperaesthesia, pruritus.

d.	Ramsay Hunt syndrome: vesicles on the pinna of the ear and facial nerve palsy due to zoster involving the geniculate ganglion.

3.	Treatment with oral acyclovir.

Infectious mononucleosis

1.	Background

a.	Also known as glandular fever.

b.	Caused by Epstein-Barr virus.

c.	Other viruses, e.g. CMV can cause IMS-like illnesses.

d.	Transmitted through oral secretions.

e.	> 95% of the population will have an EBV infection.

2.	Prodrome

a.	Long incubation period of 30 to 50 days.

b.	More often subclinical in young patients.

c.	Insidious onset with malaise, fatigue, headache, nausea, vomiting and abdominal pain.

d.	Lasts 1 – 2 weeks.

3.	Full – blown disease

a.	Fever: > 39C, not relieved by either antipyretics or antibiotics.

b.	Sore throat:

i.	pharyngitis with tonsillar enlargements and exudates.

ii.	exanthem of petechiae at junction of hard and soft palate.

c.	Hepatosplenomegaly: splenomegaly more common.

d.	Lymphadenopathy:

i.	posterior cervical lymph nodes.

ii.	epitrochlear lymph nodes.

e.	Edema of eyelids.

f.	Rashes:

i.	maculopapular erythematous rash in 20%.

ii.	withdrawal of ampicillin.

4.	Diagnosis

a.	FBC:

i.	WBC: leucocytosis – 10 – 20,000 cells/mm3.

ii.	atypical mononuclear cells: 20 – 40%.

iii.	mild thrombocytopenia: 50,000 – 200,000 / mm3.

b.	Serology:

i.	EBV-specific IgM antibodies: > 1:160 titres.

ii.	Paul-Bunnell-Davidson test.

5.	Differentials

a.	CMV infection.

b.	Toxoplasmosis.

c.	Infectious hepatitis A.

d.	Streptococcal sore throat.

e.	Diphtheria.

f.	Leukaemia and other malignancies.

6.	Complications

a.	Hepatitis: commonest complication.

b.	Splenic rupture:

i.	most feared complication.

ii.	occurs commonly during 2nd week of disease due to trauma.

c.	Swelling of the tonsils and pharynx: may lead to respiratory obstruction.

d.	CNS:

i.	meningitis: with mononuclear cells in CSF, leading to convulsions, ataxia and nuchal rigidity.

ii.	encephalitis.

iii.	transverse myelitis.

iv.	Bells palsy.

v.	Guillain Barre syndrome.

e.	Myocarditis and interstitial pneumonia.

f.	Blood:

i.	hemolytic anaemia.

ii.	thrombocytopenia purpura.

iii.	aplastic anaemia.

g.	Rare complications:

i.	pancreatitis.

ii.	parotitis.

iii.	orchitis.

iv.	Reye syndrome.

h.	Late complications:

i.	Burkitt’s lymphoma.

ii.	nasopharygeal carcinoma.

7.	Supportive therapy

a.	Bed rest.

b.	Sponge when febrile.

c.	Maintain fluid-electrolyte status.

8.	Role of corticosteroids

a.	Short course treatment:

i.	severe pharynotonsillar edema.

ii.	hepatitis.

iii.	severe abdominal pain due to splenomegaly or lymphadenopathy.

b.	Long course treatment:

i.	Guillain Barre syndrome.

ii.	hemolytic anaemia.

iii.	immune thrombocytopenia.

Dengue

1.	Background

a.	Endemic in the tropics.

b.	Caused by four dengue virus types of Flaviviridae.

c.	Principal vector: Aedes aegypti mosquito.

d.	Incubation period: 1 to 7 days.

e.	The first attack gives only partial protection against the other 3 virus types and secondary and subsequent infections are possible after a rather short time.

2.	Manifestations of the Dengue syndrome

a.	Asymptomatic.

b.	Undifferentiated viral fever.

c.	Dengue fever syndrome: with or without mild haemorrhage.

d.	Dengue haemorrhagic fever: with or without dengue shock syndrome.

3.	Dengue fever

a.	Undifferentiated febrile illness with or without maculopapular rash.

b.	Abrupt onset:

i.	high fever.

ii.	severe headache.

iii.	retro-orbital pain.

iv.	muscular and joint pain.

v.	skin haemorrhage.

c.	Mild bleeding:

i.	epistaxis.

ii.	gingival bleeding.

iii.	GI bleeding.

iv.	haematuria.

v.	menorrhagia.

4.	Dengue haemorrhagic fever

a.	The major pathophysiologic change that determines the severity of DHF and differentiates it from DF is leakage of plasma, manifested by increasing Hct and haemoconcentration.

b.	Clinical features:

Clinical sign	Features	
Fever	•	Acute onset.
•	High continuous.
•	Lasting 2 – 9 days.
•	> 41C leading to febrile convulsions.	
Haemorrhagic manifestations	Including a positive Hess test & any of the following:
•	Petechiae, pupura, ecchymoses.
•	Epistaxis, gum bleeding.
•	Haematemesis, melena.
•	Haematuria	
Hepatomegaly	•	Epigastric discomfort.
•	Right costal margin tenderness.
•	Generalized abdominal pain. 	
Shock	•	Rapid and weak pulse.
•	Narrow pulse pressure.
•	Hypotension.
•	Cold, clammy skin.
•	Restlessness.	

c.	Classically 3 types of rash seen:

i.	early febrile phase: fine petechiae scattered on extremities, axillae, face and soft palate.

ii.	convalescence: confluent erythematous + petechial rash with islands of sparing.

iii.	early / late: maculopapular / rubella-type of rash. 

d.	Danger signs

i.	abdominal pain: intense and sustained.

ii.	persistent vomiting.

iii.	hypothermia, with sweating and prostration.

iv.	restlessness or somnolence.

e.	Laboratory findings:

i.	thrombocytopenia: < 100,000 / mm3.

ii.	haemoconcentration: Hct increased by > 20% of recovery value. 

5.	Dengue shock syndrome

a.	DSS occurs with high frequency in 2 groups:

i.	children who have experienced a previous dengue infection.

ii.	infants with waning levels of maternal dengue antibodies.

b.	Onset: 3rd – 7th day after decrease in temperature.

c.	Clinical features of impending shock:

i.	sensorial changes and abdominal pain.

ii.	overt bleeding besides cutaneous bleeding.

iii.	presence of pleural effusion and ascites.

d.	Laboratory changes:

i.	increased hct by > 20%.

ii.	decreased platelet < 5 x 109 / l.

iii.	atypical mononuclear cells: > 10%.

iv.	decreased urinary sodium < 10 mmol/L.

v.	abdominal ECG.

vi.	decreased BP.

e.	Circulatory failure:

i.	skin becomes cool / blotchy / congested.

ii.	circumoral cyanosis.

iii.	increased heart rate.

iv.	lethargy and restlessness.

f.	Untreated DSS:

i.	metabolic acidosis.

ii.	severe bleeding from GIT and other organs.

iii.	intracranial haemorrhage leading to coma and death within 12 – 24 hours. 

6.	Grading of DHF

Grade	Features	
I	Non-specific constitutional symptoms.	
II	Spontaneous cutaneous bleeding in skin and other haemorrhages.	
III	Circulatory failure.	
IV	Profound shock with undetectable BP and pulse. 	

7.	Parameters for monitoring in DHF

a.	Clinical:

i.	bleeding diathesis.

ii.	symptoms suggestive of shock.

iii.	signs of fluid accumulation in 3rd space.

iv.	signs of shock.

v.	daily weight.

vi.	urinary output.

vii.	CVP.

b.	Lab:

i.	FBC.

ii.	U&E.

iii.	CXR.

iv.	ECG.

v.	PT / PTT.

vi.	ABG.

8.	Supportive therapy

a.	Intravenous fluid therapy:

i.	5% dextrose in 0.45% saline: 40 ml/kg in 1 – 2 hr reducing to 10 ml/kg.

ii.	plasma 15 – 20 ml/kg in profound shock.

iii.	cautious fresh blood transfusions in frank bleeding.

b.	Useful supportive measures:

i.	symptomatic treatment of fever.

ii.	oxygen.

iii.	iv sodium bicarbonate.

iv.	meticulous nursing care. 

Measles

1.	Background

a.	Caused by measles virus of the family paramyxoviridae.

b.	There is only one strain of the virus, and survivors of acute measles have life-long immunity.

c.	Very contagious, patients are infective during the prodromal period.

d.	Incubation period: 10 to 14 days after exposure.

2.	Prodrome

a.	Lasts 3 – 5 days. 

b.	URTI: coryza, cough and fever.

c.	Conjunctivitis.

d.	Koplik spots early in the illness on buccal mucosa: white spots surrounded by erythematous mucosa usually formed next to 2nd upper molar.

3.	Rash stage

a.	Lasts 3 days.

b.	Preceded by marked increase in fever, which subside with disappearance of rash within 3 days.

c.	Blotchy, morbiliform maculopapular rash spreads downwards from hairline to rest of body.

d.	Post-measles staining phase with “dark and dirty” brown desquamation of skin for 7 – 10 days.

4.	Complications

a.	Pneumonitis.

b.	Otitis media.

c.	Encephalomyelitis.

d.	Subacute sclerosing panencephalitis.

5.	Measles in developing countries

a.	Measles usually occurs earlier in childhood, often before 6 months of age, and can be a devastating illness.

b.	Children, particularly those who are malnourished, may die acutely from measles pneumonia, often with staphylococcal superinfection.

c.	Measles itself causes T cell immunosuppression and children with measles may develop chronic diarrhoea which exacerbates malnutrition, oral candidiasis, pneumonia. 

6.	Measles in the immunocompromised

a.	Children with pre-existing impaired T cell immunity such as those with leukaemia or with HIV infection, are at high risk from measles infection.

b.	They usually do not develop a rash.

c.	However they develop a progressive fatal pneumonitis, characterized histologically by syncytia – giant cell pneumonia. 

7.	Differentials

a.	Exanthem subitum.

b.	Rubella.

c.	Meningococcal septicaemia.

d.	Scarlet fever.

e.	Drug rash.

8.	Diagnosis

a.	Usually clinical.

b.	In atypical cases, a 4-fold rise in antibody levels.

9.	Treatment

a.	Symptomatic to relieve fever, rhinorrhoea and pruritus.

b.	Ensure adequate hydration because of fever and cough.

c.	Antibiotics for secondary bacterial infection.

d.	Consider vitamin A supplementation.

Rubella

1.	Background

a.	Caused by the rubella virus of the family Togaviridae.

b.	Also known as German measles.

c.	Currently, the main cause of morbidity ins infection in susceptible pregnant women, resulting in congenital rubella syndrome.

d.	Incubation period: 14 to 21 days after exposure.

2.	Acute infection

a.	2/3 of infections are subclinical.

b.	Mild, constitutional symptoms.

c.	Enlarged, tender retro-occipital, posterior cervical and post-auricular lymph nodes.

d.	Low grade fever and rash.

3.	Rash stage

a.	Fine maculopapular rash.

b.	Spreads downwards from face to rest of body.

c.	Disappears so fast that by the time it appears on the trunk, the face rash has disappeared.

4.	Differentiate from measles by the presence of:

a.	Milder fever and constitutional signs.

b.	Less striking rash.

c.	suboccipital lymphadenopathy.

5.	Congenital rubella syndrome

a.	Infection of mother in the 1st trimester.

b.	Results in a myriad of abnormalities:

i.	intrauterine growth retardation.

ii.	cardiac defects.

iii.	cataracts.

iv.	sensorineural hearing loss.

v.	mental retardation.

vi.	“blueberry muffin” skin lesions.

vii.	meningoencephalitis.

Mumps

1.	Background

a.	Caused by the mumps virus of the family Paramyxoviridae.

b.	Infection is rare in infancy because of persisting maternal antibodies.

c.	Transmission of infection usually occurs through direct contact with infected droplet nuclei or formites contaminated with infected saliva and possibly urine.

d.	Incubation period: 17 – 24 days.

2.	Clinical features

a.	About 1/3 of infections are subclinical.

b.	Constitutional symptoms: fever, malaise, myalgia and headache.

c.	Rapid onset of parotitis which appears 2 – 3 weeks after contact:

i.	pain and tenderness over the parotid gland.

ii.	can involve other salivary glands.

iii.	skin over parotid gland may be edematous, red and warm.

3.	Complications

a.	Meningoencephalitis: most common complication, but with a low mortality.

b.	Orchitis.

c.	Epididymitis.

d.	Pancreatitis.

e.	Arthritis.

f.	Thyroiditis.

g.	Myocarditis.

Exanthem subitum

1.	Background

a.	Mild, febrile illness caused by Human Herpesvirus 6 (HHV 6).

b.	Almost exclusively a disease of infancy: affects infants between 6 and 18 months.

2.	Clinical features

a.	Prodrome of mild URTI symptoms.

b.	Sudden onset of high fever (average 39C) that lasts for 3 – 5 days.

c.	Abrupt disappearance of fever with onset of rash 12 to 24 hours later.

3.	Rash stage

a.	fine erythematous rash.

b.	Usually centrifugal spread from trunk to extremities but never below knees.

4.	Differentiated from measles by the absence of:

a.	Constitutional symptoms.

b.	Koplik’s spot.

c.	Post-staining phase.

d.	Timing of fever and appearance of rash. 

Scarlet fever

1.	Background

a.	Caused by group A streptococcus.

b.	Commonly occurs between the ages of 5 to 15 years.

c.	Incubation period: 3 days.

2.	Clinical features

a.	Acute onset of fever, vomiting, headache, pharyngitis, chills and general unwellness.

b.	Rash appears within 12 to 48 hours after pharyngitis: fine maculopapular rash spreading from axilla and groin to rest of body.

c.	Face flushed with circumscribed pallor. 

d.	Tonsillar enlargement with exudates.

e.	White strawberry tongue: tongue coated with white exudate coat.

e.	Red strawberry tongue appears later after desquamation of the white coat.

f.	After 1 week, desquamation and peeling occurs and is extensive. 

3.	Differentiated from Kawasaki disease by:

a.	Rash on trunk and face.

b.	Extensive desquamation and peeling. 

4.	Complications

a.	Bacteraemia.

b.	Contiguous spread: sinusitis, otitis media.

c.	Rheumatic fever.

d.	Acute glomerulonephritis.

Scalded skin syndrome

1.	Caused by Staphylococcus aureus.

2.	Pattern:

a.	Initial prodrome.

b.	Rash:

i.	diffuse erythematous maculopapular rash: flaccid bullae eruptions.

ii.	extensive desquamation and peeling.

c.	Differentiated from Kawasaki disease by presence of bullae eruptions.

Toxic shock syndrome

1.	Caused by Staphylococcus aureus.

2.	Pattern

a.	Abrupt onset of high fever, vomiting and diarrhoea.

b.	Rash:

i.	appears 24 hours later.

ii.	diffuse macular.

iii.	always with hyperaemia of mucous membrane.

iv.	desquamation occurs 1 – 2 weeks later.

3.	Differentiated from Kawasaki disease by presence of:

i.	more severe systemic signs.

ii.	occurring in older children and adolescences.

Kawasaki Disease

1.	Background

a.	Also known as Mucocutaneous Lymph Node Syndrome.

b.	Febrile vasculitis of childhood: severe vasculitis of all blood vessels, especially the medium-sized vessels.

c.	An infective agent may be responsible.

2.	Epidemiology

a.	Annual incidence of 8 per 100,000 in children younger than 5 years old.

b.	More common in Asians.

c.	M:F ratio of 1.5:1.

d.	Mean age of onset: 1 – 2 years of age.

e.	Essentially a self-limiting disease, and except for the most severe coronary artery involvement, there is no long term sequelae.

3.	Pattern

a.	Acute stage:

i.	fever.

ii.	conjunctivitis.

iii.	stomatitis.

iv.	cervical lymphadenopathy.

v.	rash.

vi.	induration of peripheral extremities.

b.	Subacute phase:

i.	desquamation of skin.

ii.	thrombocytosis.

iii.	coronary artery involvement.

c.	Convalescence: coronary artery aneurysm.

4.	Diagnosis made if patient satisfy 5 out of 6 of the following:

a.	Fever:

i.	high > 38.5C.

ii.	spiking.

iii.	duration of > 5 days.

b.	Bilateral, non-suppurative conjunctivitis.

c.	Stomatitis:

i.	dry erythematous lip.

ii.	strawberry tongue.

iii.	injected oropharyngeal mucosa.

d.	Unilateral cervical lymphadenopathy (> 1.5 cm diameter).

e.	Skin:

i.	polymorphous macular erythematous rashes.

ii.	erythema multiforme.

f.	Peripheral extremities:

i.	indurated edema.

ii.	superficial desquamation of skin of hand and feet. 

5.	Complications

a.	Cardiac:

i.	coronary artery aneurysm.

ii.	myocarditis.

iii.	pericarditis.

b.	Arthralgia and arthritis.

c.	Hydrops gallbladder: abdominal pain, diarrhoea and jaundice.

d.	Uveitis.

e.	Otitis.

f.	Aseptic meningitis.

g.	Facial nerve palsy.

6.	Differentials

a.	Drug rash: Steven Johnson syndrome.

b.	Scarlet fever.

c.	Scalded skin syndrome.

d.	Toxic shock syndrome.

e.	Rheumatoid arthritis.

7.	Investigations

a.	FBC:

i.	leucocytosis.

ii.	thrombocytosis.

iii.	raised ESR.

b.	UFEME: sterile pyuria.

c.	LFT: raised enzymes.

d.	ECG: tachycardia.

e.	ECHO: coronary aneurysms.

f.	US of gallbladder.

g.	Coronary angiogram.

8.	Management

a.	Aspirin:

i.	high dose: 100 mg / kg / 24 hr for acute phase.

ii.	low dose: 1 – 3 mg / kg / 24 hr for subacute and convalescent phase up to 6 months.

iii.	if aneurysm dilatation is detected – low dose aspirin continued for years. 

b.	IV immune globulin:

i.	effective only if given within 10 days of onset.

ii.	reduces incidence of subsequent coronary aneurysm.

iii.	observe for tachycardia, hypotension, headache and vomiting. 

c.	Steroids are not indicated. 

9.	Prognosis

a.	Good for those without coronary disease.

b.	 1 – 3% get recurrent disease.

c.	20 – 25% get coronary aneurysms without IVIG, 2 – 4% with IVIG treatment.

d.	50% of coronary aneurysms resolve by 1 – 2 years. 

Henoch Schonlein Purpura

1.	Incidence

a.	Commonest acute vasculitis in childhood.

b.	Incidence of 10 – 18 / 100,000 per year.

c.	50% < 5 years, 93% < 10 years at initial presentation.

d.	Boys more commonly affected.

2.	History

a.	Preceding URTI.

b.	Rash.

c.	Arthritis and GI complaints.

d.	Haematuria.

3.	Clinical features

Clinical sign	Features	
Rash	•	Occurs in almost all patients but may not be the presenting feature.
•	Palpable purpura; may also be urticarial or maculopapular.
•	Concentrated on extensor surfaces of lower limbs, buttocks, arms and behind the eyes.
•	Pupura fades over several days & leaves a residual brown pigmentation.	
Arthritis	•	Second commonest manifestation (60 – 80%).
•	May be the presenting complaint.
•	Self-limiting and non-deforming.
•	Joints affected: knee and ankle.	
GI involvement	•	Colicky abdominal pain, vomiting and GI bleeding.
•	Rarely caused bowel infarction & perforation.
•	Intusssuception: rare but serious complication; use of air or barium enemas in investigation & treatment recommended.	
Nephritis	•	Occurs in 20% of patients.
•	Primary cause of morbidity & only manifestation that may become chronic.
•	Presentation: haematuria, proteinuria & hypertension.
•	Most manifest within 4 weeks of presentation.
•	Nephritis + nephrotic syndrome: up to 50% may develop renal failure.
•	All patients require long-term follow-up.
•	30 – 50% have persistent urinary abnormality, 1% develop ESRF.	
Others	•	Neurological: headaches, seizures, paresis.
•	GI: cholecystitis, pancreatitis.
•	GU: epididymo-orchitis.
•	Respiratory: pulmonary haemorrhages.	

4.	Diagnosis if two out of four of the following:

a.	Age < 10 years at diagnosis.

b.	Palpable purpura.

c.	Bowel angina: diffuse abdominal pain, bowel ischaemia, bloody diarrhoea.

d.	Biopsy evidence of granulocytes in the walls of arterioles or venules.

5.	Investigations

a.	FBC & ESR.

b.	LFT.

c.	Renal function tests & UFEME.

d.	Renal biopsy if nephritis is present. 

6.	Treatment

a.	Conservative:

i.	bedrest.

ii.	analgesia.

b.	Indications of steroid:

i.	abdominal pain.

ii.	orchitis.

iii.	arthritis.

iv.	nephritis (controversial).

c.	Severe nephritis: high dose methylprednisolone.

7.	Prognosis

a.	Nephritis is the only manifestation that may be chronic.

b.	All other manifestations are acute and self-limiting: the average duration of the disease is 4 weeks.

c.	There is a recurrence rate of 40%:

i.	more common in patients with nephritis.

ii.	episodes are usually milder and shorter.