Ebola virus disease

-Ebola virus is a single-stranded, nonsegmented, negative-polarity RNA virus

-It causes Ebola hemorrhagic fever (EHF)

-the virions have ‘shepherd’s crook’ appearance 

Symptoms & Signs 

-Transmission from human to human occurs via blood and body fluids

-Fever, headache, sore throat, myalgia, arthralgia, vomiting, diarrhea, rash, uveitis, shock, multiorgan failure 

Diagnosis 

-Virus is detected with a real-time RT-PCR, ELISA, and IgM antibody serum tests 

Treatment 

-There are no approved antiviral medications for treatment of Ebola virus disease

-Supportive therapy with intravenous fluids and electrolytes 

Q. What are the most common complications of EVD? Hypovolemic shock and multiorgan failure


Zika infection

Zika disease is caused by a flavivirus originally described in monkeys in the Zika Forest of Uganda in 1947

-It is transmitted by Aedes mosquitoes, sexual intercourse, and vertically from mother to child during pregnancy 

Symptoms & Signs

-Most infected individuals are asymptomatic, others can develop maculopapular rash, arthralgia,myalgia, conjunctivitis, headaches, and fever. 

-There is an increased risk of Guillain-Barré syndrome following Zika infection.

-Congenital fetal infection: greatest risk of serious fetal sequelae is with first-trimester infection; microcephaly, ventriculomegaly, intracranial calcifications, intrauterine growth restriction

Diagnosis: offer testing to any pregnant women traveling from Zika-affected regions (Central America, South America, Caribbean and Pacific Islands) 

-Real-time reverse-transcription polymerase chain reaction (rRT-PCR) testing for Zika viral RNA (in serum, urine, or whole blood) or serology

Treatment

-No specific treatment 

-Only supportive treatment: analgesics, antipyretics, mosquito prevention strategies

-Pregnancy Care: serial fetal ultrasounds every 3 to 4 weeks 

-Unlike dengue, Zika does not lead to hemorrhage or shock

Prevention

-Male patients should avoid attempts at conceiving with their partner for 6 months following symptoms or exposure

-Avoid travel to endemic areas

-Avoid mosquitoes using repellents and wearing protective clothing 

Fever, maculopapular rash + Guillain-Barré syndrome + microcephaly + history of travel to South America + caused by flavivirus which can be active in semen for up to 6 months after infection = Zika 

Anthrax bacillus

Bacillus anthracis is a gram-positive spore-forming aerobic rod

-Spores are the infectious form of the organism

-They cause a zoonotic infectious disease called Anthrax 

-the spores are inoculated through the skin, ingested, or inhaled 

-Anthrax occurs naturally in mammals and human anthrax follows exposure to infected animals or animal products or rarely bioterrorism

Symptoms & Signs 

Clinically, the disease occurs in three forms: Cutaneous, inhalational, and gastrointestinal

Cutaneous anthrax: the most common and the least morbid form of anthrax.

A painless papule progressing through vesicular, pustular, and escharotic phases resulting in painless, umbilicated ulcer (black eschar/malignant pustule); It can be associated with fever, headache, chills, cough, dyspnea, chest pain, vomiting, and fatigue. 

Inhalation anthrax: Fever, cough, dyspnea, respiratory failure, pleural effusion, hemoptysis, mediastinal edema and widening 

Gastrointestinal anthrax: nausea, vomiting, ulcers, bloody diarrhea, abdominal pain, ascites, and shock 

Diagnosis 

Culture of skin lesions, sputum, blood, and CSF

CXR: a widened mediastinum and pleural effusions

Treatment 

-Supportive care 

-Antibiotics: Ciprofloxacin, Doxycycline, Amoxicillin, Penicillin, Rifampin, Clindamycin, Clarithromycin, Erythromycin, Vancomycin, Imipenem 

Q. What is the most sensitive test for inhalational disease? Chest radiograph

Q.What is the most accurate predictor of inhalation anthrax on chest radiograph?     Mediastinal widening 


Gas Gangrene

Clostridium perfringens is a large,spore-forming, gram-positive, nonmotile rod with square ends.

-It is commonly found in the environment and intestines. 

-It produces α-toxin, a phospholipase, which causes hemolysis, tissue destruction, and shock.

-It can cause wound infections, soft tissue infections, and gas gangrene

-knife or gunshot wounds, vehicular accident wounds, surgical wounds are particularly susceptible to this bacteria 

Symptoms & Signs 

Sudden onset of excruciating pain at the affected site, brawny edema, tissue death, foul-smelling serosanguineous discharge, blisters with clear to purplish fluid, gas bubbles, crepitance, fever, hypotension, shock, and multiorgan failure 

Diagnosis: clinical history, physical examination, surgical exploration, 

Gram’s staining, and histopathologic examination. Biopsy shows gram-positive or gram-variable rods and a paucity of leukocytes. Radiographs may show gas bubbles in the tissues 

Treatment 

Gas gangrene is an emergency and requires immediate surgical debridement (excision of all devitalized tissue); administration of penicillin and clindamycin for 10–14 days

Hyperbaric oxygen therapy is controversial .

Q. What is the most effective method of prevention of gas gangrene? Surgical debridement of traumatic injuries 

Q. What is the most common adverse effect of HBO treatment? Middle ear barotrauma 


Staphylococcus epidermidis Endocarditis

Staph epidermidis thrive as Gram-positive cocci in clusters. 

-They are Coagulase-negative. Catalase-positive.

-Coagulase negative Staph are the most common cause of nosocomial bloodstream infections 

-They reside on the human skin and can enter the bloodstream at the site of intravenous catheters 

-They cause pyogenic infections on prosthetic implants such as heart valves, pacemakers, and hip joints

St-Treatment: Vancomycin plus either rifampin or an aminoglycoside.


staphylococcus aureus food poisoning

Staph aureus gastroenteritis is a common cause of food poisoning when food is left at room temperature (e.g.at picnics) 

-Foods rich in sugar (custard, cakes, ice creams), dairy, mayonnaise, potato salads, meats such as ham favor Staph growth and enterotoxin production 

-After ingestion, patients develop nausea, vomiting, abdominal cramps, diarrhea and rarely fever.

-incubation period is around 6 hours 

-Diagnosis is by history or/and by isolating S aureus or enterotoxin from the suspected food, vomitus or stool 

-Recovery is rapid usually within 24 hours; hydration if there is dehydration 


Staphylococcal Toxic Shock Syndrome

Staphylococcal toxic shock syndrome (TSS) is a toxin-mediated clinical illness characterized by rapid onset of fever, diffuse macular rash, hypotension, and multiorgan system involvement. 

-associated with tampon use, S aureus colonization of nasopharynx, vagina, rectum, wounds, abscesses 

-Symptoms are due to the production and release of exotoxins by S.aureus

Symptoms & Signs 

-Tongue is usually reddened (Strawberry tongue) 

-Subconjuntival hemorrhages 

-Fever, vomiting, watery diarrhea 

-Diffuse macular rash followed by desquamation particularly on palms and soles 

Diagnosis: Blood cultures are negative in most cases because symptoms are due to the effects of the toxin; wound cultures show S.aureus  

Treatment: Treatment of shock, antibiotic therapy, Removal of sources of toxin (eg, removal of tampon, drainage of abscess), surgical debridement 

Staph TSS vs Strep TSS: Unlike Staph TSS, Strep TSS generally lack a rash, have bacteremia and have an associated soft-tissue infection 


Staphylococcal Scalded Skin syndrome (SSSS)

SSSS is caused by hematogenous dissemination of exfoliative toxin produced by S.aureus, a toxin-producing staphylococcus

-Bullous impetigo is caused by the same exfoliative toxins when they affect the skin locally. 

-SSSS is most common in neonates and children under the age of 5 years

Symptoms & Signs: Tender, macular erythema develop abruptly over the face, axilla, and groin; as they spread, they form blisters over all parts of the body;  the blisters enlarge to slough and give ‘rolled up’ sandpaper-like texture to skin 

-Lateral traction of the skin reveals the splitting of the epidermis from the dermis (Nikolsky sign)

Diagnosis: can be established by skin biopsy and isolation of Staph aureus from the lesions 

Treatment: Antistaphylococcal antibiotics, intravenous fluids and supportive measures 

Healing occurs in 7 to 10 days.


Folliculitis due to Staphylococcus

Staphylococci are spherical gram-positive cocci arranged in irregular grapelike clusters 

-All staphylococci produce catalase, whereas no streptococci do 

-Three important species: S. aureus, S. epidermidis, and S. saprophyticus 

Staphylococcus aureus is Coagulase positive; S. epidermidis and S.saprophyticus are coagulase-negative staphylococci.

– The nose is the main site of colonization of S. aureus 

-Staphylococcus aureus causes abscesses, endocarditis, septic arthritis, and osteomyelitis, food poisoning, skin and soft-tissue infections, pneumonia, septicemia, wound infections, conjunctivitis, scalded skin syndrome, and toxic shock syndrome. 

-It is the most common cause of bacterial conjunctivitis.

Treatment: 

Abscesses: incision and drainage 

Antimicrobials: Clindamycin, trimethoprim-sulfamethoxazole, doxycycline, minocycline, dicloxacillin, cephalexin 

Folliculitis

Folliculitis is an inflammatory condition of the hair follicle characterized by groups of papules and dome-shaped pustules with central hairs 

-It can be superficial or deep 

-It can be infectious or non-infectious 

-Infections can be bacterial, viral or fungal 

-Most common bacteria causing folliculitis is Staphylococcus aureus 


Pneumococcal Meningitis

Photo by Anna Shvets on Pexels.com

Pneumococcal meningitis is caused by Streptococcus pneumoniae and is characterized by fever, neck stiffness, bulging fontanelle, irritability, and lethargy. 

-S pneumoniae is the most common cause of meningitis in adults and children 

-Individuals with splenectomy, sickle cell disease, cochlear implants are at higher risk for pneumococcal meningitis 

Symptoms & Signs: nuchal rigidity, irritability, confusion or altered mental status, headache, photophobia, nausea, vomiting, Brudzinski (neck flexion) and Kernig (straight leg raise) signs

Diagnosis: CSF culture 

Treatment: Start antibiotics within 60 minutes if bacterial meningitis is suspected; A 2-week course of intravenous antimicrobial therapy with vancomycin, ceftriaxone, cefotaxime, Penicillin G, Ampicillin 

-Survivors should be followed for neurologic sequelae like hearing loss, motor and cognitive impairment  


Erysipelas

 

Erysipelas is a sharply demarcated superficial dermal bacterial infection, most often caused by invasion of the superficial lymphatics by β-hemolytic group A streptococci (Streptococcus pyogenes) and rarely by S.aureus 

-The most common areas of infection: Legs, followed by the face 

-The most common ages affected: Infants and elderly adults 

-The lesions are red, raised, rapidly advancing with sharply demarcated margins between involved and normal tissues 

-Lesions are painful with bright red edematous indurated appearance giving rise to  “peau d’orange” appearance. 

-Facial lesions can have ‘butterfly’ pattern 

-Milian ear sign: Complete involvement of the ear by erysipelas 

-Nearly always unilateral 

Erysipelas vs.Cellulitis: Erysipelas is painful, raised, indurated plaque with sharply demarcated margins. It is superficial. 

Cellulitis may present with or without purulence


Tick-borne encephalitis (TBE)

Introduction

-Tick-borne encephalitis (TBE) is a flaviviral infection caused by TBE virus with three subtypes: European, Siberian, and Far Eastern. 

-Flaviviruses are positive-sense, single-stranded RNA, icosahedral capsid, enveloped viruses

-The principal reservoirs and vectors for TBE virus are ticks

-The virus is transmitted to humans by ticks.

-Outbreaks happened after ingestion of unpasteurized milk from infected sheep and goat  

Symptoms & Signs 

-The incubation period is 7–14 days for tick-borne exposures and only 3–4 days for milk ingestion.

-Most cases are subclinical

-The disease is characterized by a biphasic illness.

Fever-myalgia phase: Fever, arthralgia, headaches, nausea

CNS phase: headaches, meningitis, encephalitis, paralysis  

-Post-encephalitic syndrome: headaches, balance disorders, fatigue, hearing defects, attention deficits, depression, learning impairment 

Diagnosis 

Labs: leukocytosis, neutrophilia, hyponatremia 

CSF: pleocytosis 

PCR: Virus detection by RT-PCR in ticks from TBE patients 

ELISA: TBE virus IgM and IgG are detected by ELISA

Treatment 

Treatment is supportive.

Prognosis 

Complete recovery in most cases 

Prevention 

-There is no available TBE vaccine in the United States

-Effective vaccines are available in Europe, Canada and China 


Scarlet Fever

Scarlet fever is a syndrome characterized by exudative pharyngitis, fever, and scarlatiniform rash. 

-It is caused by toxin-producing group A β-hemolytic streptococci

-Symptoms and signs include sore throat, fever, rash, strawberry tongue, flushed face, and circumoral pallor 

-Rash: Diffusely erythematous rash resembling a sunburn; superimposed fine red papules give the skin a sandpaper consistency; it blanches on pressure, moves from torso to extremities, prominent on the face, chest, palms, fingers and toes; fades in 2-5 days 

-Forchheimer spots: Petechiae and punctuate red macules on the soft palate and uvula 

-Pastia lines are pink or red lines seen over the elbows and axilla during scarlet fever

-Treatment of scarlet fever is by antibiotics 




Chlamydia

Chlamydial infections

Introduction 

-Chlamydiae are obligate intracellular bacteria, possess both DNA and RNA, and have a cell wall similar to that of gram-negative bacteria.

-Chlamydiae that infect humans are divided into three species, Chlamydia trachomatis, Chlamydia pneumoniae, and Chlamydia psittaci

Chlamydia trachomatis: Chlamydia trachomatis infects only humans; incubation period: 1-3 weeks 

Eye infections: Conjunctivitis, trachoma (leading cause of preventable infectious blindness)

Lung infections: Pneumonia 

Genital infections: Urethritis, Lymphogranuloma venereum 

Joint infections: Reiter’s syndrome 

 Chlamydia pneumoniae: Chlamydia pneumoniae infects only humans; it can cause upper and lower respiratory infections 

Chlamydia psittaci: Chlamydia psittaci infects birds, humans and other animals; it causes psittacosis 

Symptoms & Signs 

Genital infection: Dysuria, urethritis, discharge, which is clearer and less purulent than seen with gonorrhea; Chlamydial infection is asymptomatic in 75% of females

Diagnosis 

Nucleic acid amplification test (NAAT): is the recommended test for screening asymptomatic at-risk and symptomatic individuals 

Culture: In culture, C. trachomatis forms intracytoplasmic inclusions containing glycogen, whereas C. psittaci and C. pneumoniae form inclusions that do not contain glycogen.

Serologic tests:  mainly to diagnose infections by C. psittaci and C. pneumoniae 

Treatment 

-All chlamydiae are susceptible to tetracyclines, such as doxycycline, and macrolides, such as erythromycin and azithromycin.

-Treatment should be offered to sex partners 

-Because of the high rate of coinfection with C.trachomatis and gonococci, any patient with a diagnosis of chlamydia should also be treated for gonorrhea and vice versa 

-Chlamydia urethritis: Azithromycin 1 g orally in a single dose or Doxycycline 100 mg orally twice a day for 7 days 

-The drug of choice for neonatal inclusion conjunctivitis and pneumonia caused by C. trachomatis is oral erythromycin. 

-The drug of choice for C. psittaci and C. pneumoniae infections and for lymphogranuloma venereum is a tetracycline such as doxycycline.

Prognosis 

Untreated chlamydia can cause serious complications 

Men: Epididymitis, sterility

Women: PID, ectopic pregnancy, infertility 

Prevention 

-There is no vaccine against any chlamydial disease

-Educate patients on safer sex practices.

Q.What are the tests of choice for the diagnosis of genital C.trachomatis infections? Nucleic acid amplification tests (NAATs) Q.What is the drug of choice for Chlamydia trachomatis sexually transmitted disease? Azithromycin



Rabies

Running German Shepherd

Introduction

Rabies is a rapidly progressive, acute, fulminant, and fatal encephalitis in humans and animals that is caused by infection with rabies virus.

-Rabies virus is usually transmitted to humans by the bite of an infected animal.

-Live virus enters the nerve tissue at the time of the bite, multiplies at the site, and then spreads centripetally along peripheral nerves toward the spinal cord or brain stem via retrograde fast axonal transport. It replicates in gray matter and then spreads  to the salivary glands, adrenal glands, and heart. 

Symptoms & Signs 

-The average incubation period is one to three months. 

-The clinical spectrum can be divided into three phases

1.Prodromal phase: 

-The first symptom is usually the paresthesia at the bite site 

-Patient later develops malaise, headache, photophobia, fever, anorexia, nausea, vomiting and sore throat 

2.Acute neurologic phase: 

Hydrophobia (fear of water), Aerophobia (fear when feeling a breeze) 

-Sympathetic overactivity (Increased salivation, ‘foaming at the mouth’, perspiration, lacrimation, pupillary dilatation, nervousness)

-Psychotic symptoms (hallucinations, delusions, bizarre behavior)

-Two acute neurologic forms of rabies are seen in humans: 

the encephalitic (furious) form in 80% and

the paralytic form in 20%.

3.Coma: Convulsive seizures, coma and death

-The major cause of death is cardiorespiratory arrest. 

Diagnosis 

1.Rabies antigens: diagnosis by rabies specific antigens 

2.Serology: Diagnosis by rabies specific antibodies,  detected by immunofluorescence or neutralization tests. 

3.Viral isolation: Isolation of the virus in the brain neurons. 

Negri bodies: the most characteristic pathologic finding in rabies; They are eosinophilic cytoplasmic inclusions in the brain or the spinal cord. They are composed of rabies virus proteins and viral RNA 

4.Animal observation: 

‘Rabid or suspected rabid’ animals: should be killed humanely immediately after the bite and sent for laboratory examination of neural tissues 

‘Normal’ animals: should be held for observation for 10 days 

If they appear abnormal during or after 10 days: kill humanely and send tissues to laboratory 

If they appear normal during or after 10 days: individualized treatment 

Prevention

Avoid contact with any unfamiliar domestic animals and wild animals 

Immunize all household dogs and high risk pets 

Vaccination: Four 1-mL doses of rabies vaccine should be given IM in the deltoid area. 

Post-Exposure Prophylaxis 

It involves wound cleaning, vaccination and passive immunity 

Wound cleaning: 

-Thoroughly clean the wound with soap and antiseptics 

-Animal bite wounds should not be sutured

Vaccination: Four doses of rabies vaccine over a 14 day period 

-Give the vaccine only in deltoid region in adults or anterolaterial thigh in children 

Never administer the vaccine in the gluteal area because antibody responses have been lower after administration at this site 

-Pregnancy is not a contraindication for immunization.

Passive immunity: One dose of HRIG along with the first dose of the vaccine 

-HRIG is not indicated beyond the 7th day after vaccination is begun, because an antibody response is most likely occurred 

-HRIG should never be administered in the same syringe or into the same injection site as the vaccine, because the antibody and vaccine will neutralize each other.

-HRIG should not be given to those with immunoglobulin A deficiency, because small amounts of immunoglobulin A present in HRIG might cause a severe allergic reaction.

Treatment 

-There is no successful treatment for clinical rabies. 

-Symptomatic and Palliative treatment using sedatives, antipsychotics, anxiolytics, and pain killers


Poliomyelitis

Poliomyelitis is a disease of the anterior horn motor neurons of the spinal cord and brainstem caused by the poliovirus. 

-Anterior horn cells control the skeletal muscle cells of the trunk and limbs 

-In up to 95% of cases, poliovirus infection is asymptomatic 

-the viral transmission is oral to oral or fecal to oral 

-Acutely, the polio virus enters the body through the GI tract, reproduces in the GI lymphoid tissue, and then spreads to the large motor nuclei of the spinal cord, the brainstem, reticular formation, hypothalamus, thalamus, cerebellum and cerebral cortex. 

Symptoms & Signs

Thankfully, not every polio infection results in paralysis. It can be divided into following types based on the severity. 

Abortive poliomyelitis: fever, headache, vomiting, diarrhea, constipation, and sore throat lasting 2–3 days.

Nonparalytic poliomyelitis: Above symptoms plus meningeal irritation and muscle spasm but no frank paralysis 

Paralytic poliomyelitis: 

Asymmetrical paralysis; Proximal limb muscles are more often involved than distal, and lower limb involvement is more common than upper. 

1.Spinal poliomyelitis: involves the muscles innervated by the spinal nerves, flaccid and weak muscles, absent tendon reflexes and fasciculations 

2. Bulbar poliomyelitis: involves the muscles innervated by the cranial nerves  IX and X; seen in up to 20 percent of polio patients with paralysis; affects swallowing, speech, facial muscles 

Post-poliomyelitis syndrome:  Fatigue, pain, respiratory problems, sleep problems, increased risk of falls 

Guillain-Barré syndrome: Always think of GBS in the differential diagnosis of polio paralysis. GBS is distinguished from polio by its symmetry, disturbances in sensation, lack of preceding aseptic meningitis, absence of a CSF pleocytosis, presence of multifocal demyelination on electrodiagnostic testing 

Diagnosis

Virus isolated and typed from throat swabs and rectal swabs; PCR amplification of poliovirus RNA from the CSF 

Treatment 

Treatment of poliomyelitis is supportive 

-Pain relief, physical therapy

-Mechanical ventilation for respiratory failure 

-Intubation or tracheostomy for secretion control 

Prevention 

the trivalent live OPV, the inactive (Salk) parenteral vaccine is currently used in the United States for all four recommended doses (at ages 2 months, 4 months, 6–18 months, and at 4–6 years).


Rubella Infection

Introduction 

Rubella is an acute febrile illness caused by Rubella virus, a single-stranded RNA virus of Togavirus family 

-It is commonly known as German measles or 3-day measles. 

-the virus enters the body through inhalation 

-it replicates in the upper respiratory tract and spreads in the bloodstream to other organs, skin and lymphoid tissues 

-the incubation period is 14 to 21 days 

-the virus has high infectivity but low virulence

Symptoms & Signs 

A.Infection in young children and adults: Fever, rash, malaise, arthralgia, lymphadenopathy, which is most prominent in the posterior cervical and postauricular areas.

Arthralgia: The most common complication of Rubella is arthralgia, and it occurs most frequently in women 

Rubella rash: A fine, pink maculopapular rash begins on the face and rapidly spreads to the trunk and extremities. It lasts for 3 days.  

B.Congenital Infection

-The greatest significance of rubella is not the acute illness but the risk of fetal damage in pregnant women. 

-the risk of fetal malformation is highest in the early stages of pregnancy 

-Intravenous immune globulin injected into the mother does not protect the fetus against rubella infection 

-The classic triad of congenital rubella consists of cataracts, cardiac abnormalities, and deafness. 

-The most common developmental manifestation of congenital rubella is mental retardation.

A.General: Failure to thrive, growth retardation, malabsorption  

B.Cerebral: Microcephaly, encephalitis

C.Ocular: Cataracts, glaucoma, microphthalmia, chorioretinitis 

D.Deafness: Sensorineural in most cases 

E.Cardiac: Pulmonary artery stenosis, pulmonary valvular stenosis,

patent ductus arteriosus, ventricular septal defect

F.Hematologic: Thrombocytopenia, lymphopenia, intravascular coagulation 

G.Skin: Blueberry muffin purpura on head, neck and trunk 

Diagnosis 

Confirmation of the diagnosis requires laboratory studies. 

A. Nucleic Acid Detection: Rubella virus nucleic acid is detected using RT-PCR 
B. Isolation and Identification of Virus: Rubella virus isolated from nasopharyngeal or throat swabs 
C. Serology: Rubella HI test 

Treatment 

Infection in young children and adults: Rubella is a mild, self-limited illness; no specific treatment is indicated; Patients should be isolated for 7 days after rash onset

Congenital infection: there is no specific treatment 

Prevention 

The primary purpose of rubella vaccination is to prevent congenital rubella infections. 

-Live attenuated rubella vaccine (MMR or MMRV) given in two doses, first dose at 12 to 15 months of age and the second dose at 4 to 6 years of age

-Pregnancy should be avoided for at least 28 days after vaccination.

-Pregnant women should not receive the vaccine, but should be screened for rubella IgG antibodies


Mumps

Introduction

-Mumps is a viral infection which primarily affects salivary glands. 

-Mumps virus is a single-stranded RNA virus and is a member of paramyxovirus family 

-The virus is transmitted by the respiratory route via droplets, saliva, and fomites.

-The highest incidence of infection is usually during the late winter and spring months, but it can occur during any season.

-It is observed to occur most frequently in the 5- to 15-year age group. 

The incubation period of mumps is ~19 days

-Viremia allows the virus to travel to all body organs, including salivary glands and central nervous system.

Symptoms & Signs 

The prodrome of mumps consists of low-grade fever, headache, anorexia malaise, and myalgia

-Hallmark of mumps: Unilateral or bilateral parotid swelling

-Other manifestations: Epididymo-orchitis, pancreatitis, acquired deafness, aseptic meningitis and encephalitis 

-Mumps during the first trimester of pregnancy increases the risk of miscarriage

Diagnosis 

-Diagnosis is made based on clinical findings or/and detection of viral RNA by reverse-transcriptase PCR (RT-PCR) or viral culture 

Treatment 

-Mumps is a self-limited, usually mild, disease. 

-Treatment is supportive and consists of antipyretics, fluids, and analgesics. 

-Stay home from school or work for 5 days after symptom onset.

Prevention 

-Usually Natural infection confers life-long protection

The MMR vaccine is given routinely subcutaneously to all healthy children at age 12–15 months with a second dose at age 4–6 years.

-Mumps vaccine contains live attenuated virus. It is not recommended for pregnant women