Viral Infections
Dr Ban Abdul Hammed Pediatrics DepartmentMeasles
Measles:- is an acute viral infection caused by Measles virus which is an RNA virus of the genus Morbillivirus in the family Paramyxoviridae. Transmission:- Measles is highly contagious disease. Maximal dissemination of virus occurs by droplet spray during the prodromal period (catarrhal stage ). During the prodromal period and for a short time after the rash appears , the virus is shed in nasopharyngeal secretions, blood, and urine. Infants acquire immunity transplacentally from mothers. this immunity is usually complete for the first 4-6 month of life.Measles
Clinical Manifestations :- Measles has three clinical stages :- 1- An incubation period stage. 2- Prodromal stage. 3- Final stage with maculopapular rash. The incubation period lasts about 10-12 days to the first prodromal symptoms. The prodromal stage lasts 3-5 days and is characterized by low grade fever, dry cough, coryza and conjunctivitis. these symptoms precede the appearance of KOPLIK SPOTS( the patho gnomonic sign of measles) by 2-3 days.MEASLES
KOPLIK SPOTS :- are grayish white dotes, as small as grains of sands, that have reddish areolae.they tend to occur on the inner aspects of the cheeks at the level of premolars, but may spread over the rest of buccal mucosa. they disappear with in 12- 18 hr. The conjunctival inflammation and photophobia may suggest measles before koplik spots appear. the temperature rises abruptly as the rash appears and often reaches 40c. The rash starts as faint macules on the upper lateral parts of the neck, behind the ears, and on the posterior parts of the cheek. the rash becomes maculopapular as it spread to involve other parts of the body. finally it reach the feet on the 2-3rd day usually with abrupt drop in body tempters. rash fades downwards in the same sequence in which it appears. The severity of disease is directly related to the extend and confluence of the rash.
Clinical manifestations of measles
In sever cases petechaie may be present in large numbers and there may be extensive echemosis. Lymph nodes may be enlarged and slight splenomegaly may be noted.Mesentric lymphadenopathy may cause abdominal pain. Otitis media ,bronchopneumonia and GIT symptoms such as diarrhea and vomiting are more common in infant and small children. Patients with measles are infectious from 3 days before the rash up to 4- 6 days after its onset. The rash of measles fades over about 7 days.Measles
Differential diagnosis :- 1- Rubella 2- Roseola infantum 3- Scarlet fever. 4- Infectious mononucleosis. 5- meningococcemia. 6- Infection result from adeno and enteroviruses. 7- Drug rash.Measles
Diagnosis :- Diagnosis is usually apparent from the characteristic clinical picture, laboratory confirmation is rarely needed. The Lab investigations include 1- measurement of Measles IgM antibodies titer. IgM antibody appears in serum 1-2 days after the onset of the rash and remains for about 1 month. 2- isolation of measles virus from blood, urine, nasopharyngeal secretions . 3- WBC tends to be low with relative lymphocytosis.Measles
Treatment :- There is no specific antiviral therapy. Treatment is supportive by 1- anti pyretics (acetaminophen) for fever. 2- Bed rest. 3- Maintenance of adequate fluid intake. 4- Humidification may alleviate symptoms of laryngitis or irritating cough. 5- patient with photophobia should be protected from exposure to strong light. 6- Bacterial complications of otitis media & bronchopneumonia require antimicrobial therapy. 7- treatment with vitamin A reduces the morbidity and mortality in children with sever measles. Single dose of 100000 I.U orally for children (6m- 1 y ) and 200000 I.U for older children.Measles
Complications :- 1- Otitis media. 2- Pneumonia: it is either interstitial pneumonia caused by measles virus(giant cell pneumonia ) . Or it is caused by bacterial super infection (bronchopneumonia) with pneumococcus ,group A streptococcus or staph. 3- Croup,tracheitis,and bronchiolitis are common complications in infants. 4- Myocarditis. 5- exacerbation of underlying mycobacterium tuberculosis. 6- Neurological complications .the most common is encephalitis which occur 2-5 days after appearance of rash.Measles
Complications of measles :- Other neurological complications include Guillain- Barre syndrome,hemiplegia and cerebralthrombophlebitis. 7- Sub acute sclerosing panencephalitis. It is a chronic encephalitis caused by persistent measles virus infection of the central nervous system.Measles
Prevention :- 1-Isolation precautions in hospitals and other institutions should be maintained from7th day after exposure until 5 days after the rash has appeared. 2- Vaccine:- The initial measles immunization usually as measles – mumps-rubella (MMR) vaccine is recommended at 12- 15 mo of age . A second immunization is recommended at 4-6 yr.
Measles
Prevention of measles :- 3- Post exposure prophylaxis : Passive immunization with immune globulin is effective for prevention and attenuation of measles with in 6 days of exposure. Susceptible house hold and hospital contact who are younger than 12 month of age or who are pregnant, should receive immune globulin (0.25 ml / kg) I.M with in 5 days after exposure. Immunocompromised persons should received immune globulin (0.5 ml / kg ) I.M regardless of immunization status after exposure to measles.MEASLES
Koplic spotsMAESLES
Measles rashRUBELLA
Rubella ( German or three- day measles ) Etiology :- Rubella virus, the cause of rubella is an RNA virus of the genus Rubivirus in the family togaviridae. Epidemiology :- Humans are the only natural host of rubella virus, which is spread either by oral droplet or transplacentally to the fetus causing congenital infection.Rubella
During clinical illness the virus is shed in nasopharyngeal secretions, blood, feces and urine. virus has been recovered from nasopharynx 7 days before exanthem and 7-8 days after its disappearance. Clinical manifestations :- The incubation period is 14- 21 days. The prodromal symptoms are mild. The most characteristic sign of rubella is retro auricular, post cervical and post occipital lymph adenopathy . The lymph nodes are tender and appear 24 hr before the rash start .they may remain for one week. An enanthem appears just before the onset of the rash .it consists of rose colored spots on the soft palate.Rubella
The exanthem ( the rash ) begins on the face and spread quickly. It may be fade on the face by the time it appears on the trunk The rash is maculopapular with flushing. The rash spreads over the entire body with in 24 hr.during the second day the rash assume a pinpoint appearance. mild itching may occur. The rash usually clears by third day . There is no photophobia , fever is low grade during the rash and persist for 1-3 days . The spleen is often slightly enlarged .In older girls polyarthritis with arthralgia may occur .Rubella
Diagnosis :-The diagnosis of rubella may be apparent from clinical symptoms. But it is usually confirmed by serology or viral culture .1- Serology :- Hem agglutination – inhibition ( HI) antibody has been the reference method of determining immunity to rubella. latex agglutination , enzyme immunoassay and fluorescent immunoassay are also useful.Immunoglobulin IgM antibodies are detected in the first few days of illness and are considered diagnostic .fourfold increase in IgG titer is also diagnostic.
Diagnosis of Rubella
2- Culture :- rubella virus can be cultured from nasopharynx and blood . 3- CBP:- the WBC is normal or slightly reduced. Mild thrombocytopenia have been described. Differential Diagnosis:- 1- Measles 2- Roseola infantum. 3- Scarlet fever. 4- Infectious mono nucleosis. 5- Drug rash . The period of highest communicability is from 5days before the rash to 6 days following appearance of the rash.Rubella
Treatment :- No specific anti viral therapy , treatment is supportive . Complications :- 1- Encephalitis. 2- Thrombocytopenic purpura. 3- Arthritis. 4- Progressive rubella pan encephalitis.Congenital Rubella Syndrome
Congenital rubella syndrome :- it affects all organ systems, the most common manifestation is intrauterine growth retardation. Other common findings include cataract, microphthalmia. Myocarditis,structural cardiac defects ( patent ductus arteriosus or pulmonary artery stenosis ).sensorineural deafness.meningoencephalitis and blueberry muffin skin lesion. Persistent infection lead to pneumonia, hepatitis, bone lucencies , anemia and thrombocytopenic purpura.patient may have enlargement of liver and spleen. Later sequelae include motor and mental retardation.Rubella
Diagnosis of congenital rubella syndrome:- The diagnosis is confirmed by finding rubella specific IgM antibodies in the neonatal serum. or by culturing rubella virus from the infant ( nasopharynx, urine, or tissue ).prenatal diagnosis of fetal rubella can be made either by isolating the virus from amniotic fluid or by rubella specific IgM antibody in cord blood.Rubella
Prevention of rubella :-Prevention of rubella is by vaccination .The initial rubella immunization, usually as measles – mumps- rubella ( MMR ) vaccine .it is recommended at (12 -15 mo ) of age .A second immunization also as MMR is recommended at age 4-6 yr .children who have not received this second dose should be immunized by 11-12 yr of age .Mumps
Etiology :- Mumps virus is RNA virus of the genus paramyxovirus in the family paramyxoviridea. Epidemiology :- The virus is spread from person to others by respiratory droplets. Maximum transmission of the virus occur 1-2 days before the appearance of the swelling until 5 days after parotid swelling. Mumps infection occurred more often in the winter and spring months.Mumps
Clinical Manifestations :- The incubation period is ( 14- 24 ) days. About 30- 40 % of infection is sub clinical. In children prodromal manifestations are rare but may be manifested by fever, headache and pain in the neck. The involvement of salivary glands are characterized by pain and swelling in one or both parotid glands. The parotid swelling first fills the space between the post boarder of the mandible and the mastoid and then extends down ward and fore ward. the swollen tissues push the ear lobe up ward and outward .
Mumps
The swollen area is tender and painful, pain being elicited by testing sour liquids such as lemon juice. Edema of the homolateral pharynx and soft palate may occur with displacement of the tonsil medially. One parotid gland usually swells a day or two before the other. The parotid swelling subsided with in 3-7 days. Although the parotid glands alone are affected but swelling of submandibular glands and less commonly sublingual glands may occur .Mumps
Diagnosis :- The diagnosis of mumps is usually apparent from the clinical symptoms and examination. routine laboratory tests are non specific , usually leucopenia is present with relative lymphocytosis. An elevation of serum amylase level is common . The microbiologic study is by 1- serology. 2- virus culture. Serology :- Enzyme immunoassay for mumps immunoglobulin IgG, IgM antibodies are commonly used for diagnosis. Mumps virus can be cultured from the saliva, cerebrospinal fluid, blood and urine.Mumps
D. diagnosis :- 1- Other viral causes of parotitis ,include HIV, influenza, parainfluenza viruses. 2- Acute suppurative parotitis by staphylococcus aureus. 3- Salivary calculus obstruction. Treatment :- There is no specific antiviral therapy , treatment is supportive. - Antipyretics are indicated for fever. - Bed rest. - The diet should be adjusted to the patient ability to chew. - Orchitis should be treated with local support and bed rest.Mumps
Complications :- 1- Meningoencephalitis :- it is the most common complications .the cerebrospinal fluid examination may show increase cell count ( less 500 cells / mm) mainly lymphocyte. protein 50-200 mg/dl. Glucose usually normal but may decrease to 40mg/dl. 2- Orchitis and Epididymitis :- it is usually follows parotitis with in 8 days. The onset is abrupt with fever ,nausea and lower abdominal pain. the affected testis become swollen and tender. 3- Pancreatitis. 4- Myocarditis. 5- Arthritis. 6- Thyroiditis. 7- Deafness 8- Ocular complications ( optic neuritis, dacryadenitis.) 9- Oophoritis. 10-Thrombocytopenia.(uncommon)Mumps
MumpsVaricella (chickenpox )
Varicella – zoster virus (VZV ) causes primary, latent, and recurrent infections.The primary infection is manifested as Varicella (chickenpox ) and result in establishment of a lifelong latent infection of sensory ganglion neurons .Reactivation of the latent infection causes herpes zoster (shingles ). Herpes zoster because it is due to the reactivation of latent VZV so it is uncommon in childhood .Varicella
Epidemiology :- Patients with varicella are contagious from 24- 48 hr before the rash appears and until the vesicles are crusted , usually 3-7 days after onset of rash. VZV is transmitted in respiratory secretions and in the fluid of skin lesions either by airborne spread or through direct contact.
Varicella
Clinical Manifestations :- The incubation period range from 10- 21 days. Prodromal symptoms include fever, malaise, anorexia and occasionally mild abdominal pain may occur 24-48 hr before the rash appears. Varicella lesions appear first on the scalp ,face or trunk. the initial exanthem consists of intensely pruritic erythematous macules that evolve through the papular stage to form clear fluid-filled vesicles. While the initial lesions are crusted ,new crops form on the trunk and then the extremities. The simultaneous presence of lesions in various stages of evolution is characteristic of varicella.Varicella
The distribution of the rash is predominantly central . Many children have vesicular lesions on the eyelids and conjunctivae, but corneal involvement is rare.hypopigmentations or hyper pigmentation of lesions sites persist for days or weeks but sever scaring is unusual unless the lesions were secondary infected. Ulcerative lesions involving the oropharynx are also common.Varicella
Differential diagnosis :- 1- vesicular lesions by herpes simplex virus. 2- staphylococcus aureus skin lesion. 3- contact dermatitis. 4- drug rash. 5- insect bites. Diagnosis :- Diagnosis is usually depend on clinical examination and lab evaluation is only important in high risk patients. 1- VZV can be identified by direct fluorescence assay (DFA ) of cell from cutaneous lesion. 2- virus can be recovered by using tissue culture methods. 3- VZV immunoglobulin (IgG ) can be detected , and 4- folds rise in IgG level confirm the diagnosis of acute infection. 4- WBC is decrease with lymphocytosis.Varicella
Treatment :- Antiviral drug used is acyclovir. Oral acyclovir (20 mg / kg / dose maximum 800 mg/ dose ) given as 4 doses per day for 5 days. Should be used to treat uncomplicated varicella. Intravenous acyclovir is indicated for sever disease , immunocompromised patient, pregnant women with varicella and any patient who has signs of disseminated VZV including (pneumonia, sever hepatitis, thrombocytopenia or encephalitis.) the dose of intravenous acyclovir is ( 500mg/m2 given 8hourly). treatment is continued for 7 days. If therapy initiated within 72 hr of development of initial symptoms this will decrease the likelihood of progressive varicella in high risk patient .Varicella
Complications :- 1- secondary bacterial infections of the skin usually by streptococcus and staphylococcus. 2- encephalitis and cerebellar ataxia. Neurological symptoms usually begin 2-6 days after the onset of the rash but may occur during the incubation period or after resolution of the rash. 3- pneumonia . Varicella pneumonia is a sever complication . The respiratory symptoms of cough,dyspnea, cyanosis and pleuritic chest pain usually begins within 1-6 days after the onset of the rash. 4- hepatitis. 5- thrombocytopenia. 6- other rare complications include nephritis, nephrotic syndrome,arithritis, Myocarditis, pericarditis, Pancreatitis and Orchitis.Varicella
Prevention:-1-isolation of infected patient.2- Vaccine:- live virus vaccine to prevent varicella is recommended at 12-18 month of age and at 4-6 years.3- post exposure prophylaxis:- varicella–zoster immunoglobulin ( VZIG ) post exposure prophylaxis is recommended for immunocompromised patient, pregnant women and new born exposed to maternal varicella.Chicken pox
Varicella
Infectious mononucleosis (glandular fever )Etiology :- Epstein- Barr virus (EBV ) causes more than 90% of infectious mononucleosis cases. about 5-10% of infectious mononucleosis like illnesses are caused by cytomegalovirus, toxoplasma gondii, adenovirus, viral hepatitis and HIV. Epidemiology :- The virus is transmitted in oral secretions by close contact such as kissing. EBV is shed in oral secretions for 6 month after acute infection and then intermittently for life. EBV is also found in the genital tract of women and may be spread by sexual contact.
Infectious mononucleosis (glandular fever )
Pathogenesis :- EBV initially infects oral epithelial cells, this may contribute to the symptoms of pharyngitis.then it spread to other structures like salivary glands. With development of viremia ,B lymphocyte infected and the entire lymphoreticular systems , including the liver and spleen. The a typical lymphocytes that are characteristic of IMN are CD8+ T lymphocytes which exhibit both suppressor and cytotoxic functions that develop in response to the infected B lymphocytes. EBV establishes life long latent infection after the primary illness. the latent virus is carried in oropharyngeal cells and systemic B lymphocyte.Infectious mononucleosis
Clinical Manifestations :- The incubation period of IMN in adolescents is 30-50 days. In children it may be shorter. The majority of cases of EBV infection in infants and young children are clinically silent. Patients may complain of malaise, fever, fatigue, headache, sore throat, abdominal pain and myalgia.This prodromal manifestations may last 1-2 wk. The complaints of sore throat and fever gradually increase until patients seek medical care.Infectious mononucleosis
Clinical Manifestations :- The physical examination is characterized by generalized lymphadenopathy, splenomegaly and hepatomegaly. Lymphadenopathy occurs most commonly in the anterior and posterior cervical lymph nodes.Epitrochlear lymphadenopathy is suggestive of IMN.splenomegaly to 2-3 cm below costal margin is typical . Massive enlargement is uncommon. Symptomatic hepatitis or jaundice is uncommon. The sore throat is often associated with pharyngitis, tonsillar enlargement occasionally with exudates.petechiae at the junction of the hard and soft palate are frequently seen. other clinical findings may includes skin rash and edema of the eyelids. the rash is maculopapular and reported in 3-15% of patients. up to 80% of patients of IMN develop Ampicillin rash if treated with ampicillin or amoxicillin . This rash is immune mediated and resolve with out treatment. The major symptoms typically last 2-4 weeks.Infectious Mononucleosis
Infectious mononucleosisDiagnosis :-A presumptive diagnosis can be made by the presence of typical clinical symptoms with a typical lymphocytosis in the peripheral blood. The diagnosis can be confirmed by serologic testing.1- Routine laboratory tests:-C.B.P reveals leukocytosis of 10000-20000cells/mm3. of which at least two third are lymphocytes. A typical lymphocytes account for 20-40%of the total number. The a typical cells are mature T lymphocytes that have been antigenically activated. Compared with regular lymphocytes microscopically , atypical lymphocytes are larger overall, have larger eccentrically placed nuclei with lower nuclear to cytoplasm ratio.Platelet count may decrease. Mild elevation of hepatic transaminase occur in 50% of the cases. 2- Heterophile Antibody tests:- heterophile antibodies agglutinate cells from species different from those in the source serum. these are IgM antibodies detected by Paul- Bunnell – Davidsohn test for sheep red cells agglutination
Infectious mononucleosis
3- Specific EBV Antibodies :- EBV specific antibodies testing is useful to confirm acute and past infection. The EBNA ( nuclear antigen ), EA ( early antigen ) , and VCA ( viral capsid antigen ) These are most useful for diagnosis. The acute phase of infection is characterized by rapid IgM and IgG response to VCA in all cases and an IgG response to EA in most cases. The detection of IgM antibody to VCA is the most valuable and specific serologic test for the diagnosis of acute infection. Anti EBNA antibody are the last to develop and gradually appear 3-4 month after the onset of illness and remain for life. Presence of anti-EBVA antibody implies infection occurring more than 3-4 month previously.Infectious mononucleosis
Treatment :- 1- therapy with high dose of acyclovir decrease viral replication and oropharyngeal shedding but not reduce the severity or duration of symptoms. 2- Bed rest and symptomatic therapy are the mainstays of management. 3- Because blunt abdominal trauma may predispose patients to splenic rupture so it is important to advise against participation in contact sports and strenuous athletic activities during the first 2-3 wk of illness. 4- Short courses of corticosteroids ( less than 2 wk ) may be helpful for complications of IMN. The indications for steroid therapy include :- A- incipient upper air way obstruction. B- thrombocytopenia C- autoimmune hemolytic anemia. D- seizures and meningitis. A recommended dose is prednisone 1mg/ kg / 24 hr.for 7 days and tapered over another 7 days.Infectious mononucleosis
Complications :- 1- the most feared complication is sub capsular splenic hemorrhage or splenic rupture, which occur most frequently during the second week of the disease. 2- swelling of the tonsils and oropharyngeal lymphoid tissue may cause air way obstruction 3- Neurological complications :- include headache, seizures, ataxia,meningitis,encephalitis and facial nerve palsy. 4- Hemolytic anemia. 5- A plastic anemia. 6- Thrombocytopenia and neutropenia. 7- Myocarditis. 8- Interstitial pneumonia. 9- Other rare complications include Pancreatitis, parotitis and Orchitis.Roseola infantum
Roseola infantum or (Exanthem subitum ) Or sixth disease. Etiology :- it is caused by human herpes virus-6 ( HHV-6 and less frequently by human herpes virus -7 (HHV-7) Epidemiology :- Roseola can develop in children year around but higher incidence occur during spring and fall months. Peak acquisition of primary HHV-6 infection from 6-15 month of age. Most adult excrete HHV-6 in saliva and may serve as primary sources for viral transmission to children. There is evidence that HHV-6 can be transmitted in utero but this is rare and no malformations have been noted.Roseola
Clinical Manifestations :- Roseola is a mild febrile illness occurring during infancy with peak at 6- 15 month of age. Transplacental antibodies protect most infant until 6 month of age. The incubation period about ( 5- 15 )days. The prodromal period include mild rhinorrhea , slight pharyngeal inflammation, mild conjunctival redness and mild cervical or occipital lymphadenopathy. Patient usually develops high fever, the temperature range from (37.9- 40 c. Some children may become irritable and anorexic . Seizures may occur in 5-10 % of children during this febrile period. Fever persists for 3-5 days, and then typically resolves abruptly or gradually diminished over 24-36 hr.A rash appears with in 12-24 hr of fever resolutions. The Roseola rash begins as discrete ,small, slightly raised pink lesions on the trunk then spreads to neck, face and proximal extremities. the rash is not pruritic.the rash of roseola is rose colored , as the name implies. After 1-3 days the rash fades.
Roseola
Diagnosis :- The most important reasons for establishing the diagnosis of Roseola is to differentiate this mild illness from other serious rash like measles. The diagnosis usually depends on history and clinical findings. Laboratory findings include :- during the period of exanthem the WBC decrease with relative lymphocytosis. Specific tests for diagnosis of HHV-6 infection include serology, virus culture, antigen detection, and polymerase chain reaction(PCR ). D.Diagnosis :- 1- Measles :- the appearance of rash in measles occur with the height of fever , as well as the presence of cough, conjunctivitis, and koplik spots. 2- Rubella. 3- Scarlet fever. 4- Enteroviruses. 5- Drug hypersensitivity.Roseola
Treatment :- 1- Supportive treatment in form of acetaminophen, for fever. and adequate fluid intake. 2- Referral to hospital should be considered in those with serious complications like encephalitis, pneumonia, and hepatitis. 3- The generally benign nature of Roseola precludes utilization of antiviral therapy. but this therapy may be considered in children with neurological complication, and immunocompromised patient.HHV-6 infection inhibited by ganciclover, cidofovir, and foscarnet. But NOT acyclovir.Roseola infantum
RoseolaPolioviruses
Etiology :- polioviruses are RNA viruses belong to the bicornaviridea family in the genus Enterovirus and include three serotypes ( type 1,2,3 ). Polioviruses spread from the intestinal tract to the central nervous system, where they cause aseptic meningitis and poliomyelitis or polio. Transmission :- Humans are the only known reservoir for the viruses. polio virus has been isolated from the feces more than two weeks before paralysis to several weeks after the onset of symptoms. The disease is spread by direct contact with infected person through pharyngeal secretions or by contaminated feces (fecal- oral spread ).Polio
Pathogenesis :- Poliovirus enters the body via the oral route , it multiply in the tonsillopharyngeal tissue then it pass to regional lymph nodes. The virus reach the to the intestinal tract and multiply there. it pass to blood stream then it reach to the CNS.the main pathological lesion in the CNS involve motor neuron cells in the spinal cord ( the anterior horn cells ) and the medulla oblongata ( the cranial nerve nuclei ).Polio
Clinical Manifestations :- The incubation period of poliovirus is 8-12 days. with range of 5- 35 days. poliovirus infections may follow one of several courses :- 1- in apparent infection. 2- abortive polio. 3- non paralytic polio. 4- paralytic polio. 1- in apparent infection :- occurs in 90-95% of cases and causes no disease and no sequelae. 2- abortive poliomyelitis :- occurs in 5% of cases. The patient develops fever, malaise, anorexia and headache. there may be sore throat, abdominal pain and vomiting. The physical examination is normal, recovery is complete. the duration of illness is 2-3 days.Poliomyelitis
Clinical Manifestations :- 3- Non paralytic polio :- occurs in 1% of cases. Patients present with headache, nausea, vomiting and stiffness of the neck, trunk and limbs. Fleeting paralysis of the bladder and constipation are frequent.approximatly two thirds of these children have a short symptoms free interlude between the first phase ( minor illness ) and the second phase ( CNS disease or major illness ) .During the second phase patients develop nuchal and spinal rigidity with positive kernig sign and neck rigidity. In the early stages the reflexes are normally active and remain so unless paralysis occur. Changes in the reflexes may precede weakness by 12-24 hr. The superficial reflexes are usually first to diminished . Changes in deep tendon reflexes occur 8-24 hr after the superficial reflexes are depressed and indicate impending paresis of extremities. Sensory defects do not occur in polio.
Polio
Clinical Manifestations :- 4- Paralytic poliomyelitis :- it develops in 0.1% of all cases. it cause three clinically recognized syndromes these are A- spinal paralytic polio. B- bulbar polio. C- polio encephalitis. A- spinal paralytic polio :- it has two phases .in the first phase patient develops fever, anorexia, and head ache. Then the patient feels well for 2-5 days. After that patient develops sever headache , fever, and sever muscle pain. on examination there is neck rigidity, hyperactive deep tendon reflexes initially followed by absence or diminished reflexes. With in 1-2 days asymmetric flaccid paralysis occurs. Involvement of one leg is most common, followed by involvement of one arm. there is also weakness of muscle of the neck, abdomen , trunk, diaphragm and thorax. sensation is intact. Paralysis of limbs is often accompanied by bowel and bladder dysfunction.Polio
Spinal paralytic poliomyelitis:- The return of strength and reflexes is slow and may continue to improve as long as 18 months after the acute disease. Lack of improvement from paralysis with in the first several weeks or months ( about 6 months) after onset is usually evidence of permanent paralysis. Atrophy of the limb, failure of growth and deformity is common in paralytic limb.Polio
Bulbar polio :- It may occur as a clinical entity with out apparent involvement of the spinal cord. The clinical findings seen with bulbar polio include :- 1-paralysis of extra ocular, facial, and masticatory muscles. 2- nasal twang to the voice caused by palatal and pharyngeal weakness. 3- inability to swallow smoothly. 4- accumulation of pharyngeal secretions which may cause irregular respiration. 5- absence of effective coughing. 6- nasal regurgitation of saliva and fluids as a result of palatal paralysis. 7- involvement of vital centers in the medulla which are manifested by irregularity in rate, and rhythm of respiration. and cardiovascular alteration include increase in blood pressure. and cardiac arrhythmias. 8- paralysis of one or both vocal cords causing hoarseness of voice , aphonia, and asphyxia.Polio
Bulbar polio :- the course of bulbar polio variable , some patients die as a result of extensive involvement of vital centers in the medulla. Others recover partially with respiratory support, and others recover completely . Cranial nerves involvement is seldom permanent. Polio encephalitis :- it is a rare form of the disease in which higher centers of the brain are severely involved. Irritability , seizure, coma, and spastic paralysis, with increase reflexes may be observed. Peripheral and cranial nerves paralysis may occur . Hypoxia and hypercapnia may caused by inadequate ventilation.Polio
Diagnosis :- In suspected cases of acute flaccid paralysis 2 stool specimens should be collected 24 -48 hr apart if the diagnosis of polio is suspected. Polio virus can be isolated from stool sample especially during the first week after the onset of paralysis. The CSF is normal during minor illness but with CNS involvement there is pleocytosis between 20-300 cells mainly lymphocytes. Protein is elevated to 50- 100mg/dl. Serologic test demonstrate increase in antibody titer during acute phase of illness and 3-6 wk later.Polio
Treatment:- There is no anti viral agent for treating polio. All intramuscular injections and surgical procedures are contraindicated during the acute phase of illness especially during the first week because these may result in progression of disease. Treatment of abortive polio:- Supportive treatment with analgesic, proper diet, and bed rest. A proper neurological examination should be done for those patients 2 months later. Treatment of Non paralytic polio :- Analgesic with application of hot packs for relieve muscular discomfort. Proper neurological examination should be done after 2 months. Treatment of paralytic polio :- Most patients need hospitalization. Complete rest for 2-3 weeks. Suitable body alignment is necessary to prevent skeletal deformity.Polio
Treatment of paralytic polio :- Moist hot packs may relieve muscle pain and spasm. Constipation is common and fecal impaction should be prevented. A proper diet and high fluid intake should be started. Active and passive motion are indicated as soon as the pain has disappeared. If permanent paralysis of the limb occur this may need a skilled orthopedic advice. and regular physiotherapy . The extent of paralysis is directly related to the extent of neuronal involvement , paralysis occurs if more than 50% of the neurons are destroyed .