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Home , Infectious mononucleosis

د. أسيل Lec. 4 سامي Poliomyelitis Etiology: are RNA belonging to the Picornaviridae family, in the genus Enterovirus. Epidemiology:  90–95% of are unapparent  Clinically apparent but non-paralytic illness occurs in about 5% of all infections  Paralytic occurs in about 1/1,000 infections among infants to about 1/100 infections among adolescents.  Polio was eradicated from most of world.  Humans are the only known reservoir for the polioviruses  has been isolated from feces for >2 wk before paralysis to several weeks after the onset of symptoms.  The of poliovirus is 8–12 days : spread by the fecal-oral route. Pathology & Pathogenesis : The primary site of replication is in the mucosa of the small intestine. Regional lymph nodes are infected, and primary viremia occurs after 2–3 days. The seeds multiple sites, including the CNS, reticuloendothelial system, brown fat deposits, and skeletal muscle. The exact mechanism of entry into the CNS is not known, however, the virus may traverse neural pathways, and multiple sites within the CNS are often affected. Clinical picture : 4 forms: 1. Inapparent polio (90 – 95%): no disease and no sequelae.

1 2. Abortive polio (5%) : , , anorexia, and . occurs irregularly. Recovery is complete, and no neurologic signs or sequelae develop. 3. Non-paralytic polio (1%) : same picture as abortive more intense headache, , and vomiting, as well as soreness and stiffness of the posterior muscles of the neck, trunk, and limbs. Changes in reflexes, either increased or decreased, may precede weakness by 12–24 hr. ⅔ of these children have a short symptom-free interlude between the 1st phase (minor illness) and the 2nd phase (CNS disease or major illness). Constipation & retention may occur. They also recover. 4. Paralytic polio (0.1%) : come in 3 forms: A. Spinal paralytic poliomyelitis: starts as abortive, recovery for 2–5 days, then fever, aches & asymmetric flaccid paralysis occurs. Paralysis may be permanent or may recover slowly. B. Bulbar poliomyelitis: involvement of stem with cranial nerves dysfunction leading to respiratory & swallowing difficulties. It may recover completely or partially & rarely permanent. C. Polioencephalitis : rare form of the disease present as any viral

Mixed forms of 2 of these forms exist. Diagnosis & Investigations : In suspected cases of acute flaccid paralysis, 2 stool specimens should be collected 24–48 hr apart, as soon as possible to diagnose by DNA sequence analysis & viral culture. with CNS involvement CSF demonstrates a pleocytosis of 20–300 cells/mm3 of mainly. Treatment : There is no specific antiviral treatment for poliomyelitis. Most patients with the paralytic form require hospitalization with complete physical rest in a calm atmosphere for the 1st 2–3 weeks. Monitoring of swallowing & respiratory movements is needed & problems should be dealt with. The rest of treatment is supportive with , sedatives, diet, and bed rest.

Complications : 2 a) Acute gastric dilatation b) superficial intestinal erosions c) problems of immobilization d) paralysis of bowel & bladder e) problems of swallowing & aspiration f) respiratory problems & paralysis Prevention : A. vaccination B. Hygienic measures Infectious mononucleosis : Etiology : Epstein Barr virus is DNA virus from herpes family. Epidemiology :  EBV Infection is common in infancy & early childhood, while the classic triad of , , & generalized is rarely seen in children <4 years of age.  The incubation period of infectious mononucleosis in adolescents is 30–50 days. In children, it may be shorter. Transmission : It is transmitted via saliva like kissing. Pathogenesis : EBV initially infects oral epithelial cells then it spreads to near structures with eventual viremia and infection of B-lymphocytes in the peripheral and the entire lymphoreticular system, including the and . EBV establishes lifelong latent infection in oropharyngeal epithelial cells and B-lymphocytes & reactivation is asymptomatic but is source of infection to others. Clinical picture :  The majority of cases of primary EBV infection in infants and young children are clinically silent.  In older patients, the onset of illness is usually insidious with malaise, fatigue, acute or prolonged (>1 wk) fever, headache, , nausea, , and lasting 1-2 weeks.

3  They main signs are generalized lymphadenopathy (90% of cases){mainly cervical}, (50% of cases), and (10% of cases).  Symptomatic or is uncommon, but elevated liver enzymes are common.  There is usually marked tonsillar enlargement.  Up to 80% of patients with infectious mononucleosis experience “ ” if treated with ampicillin or & other also may occur.  The major symptoms typically last 2–4 wk, followed by gradual recovery. Investigations : i. with atypical in the blood. ii. diagnosis is usually confirmed by serologic testing, either for heterophile (Paul-Bunnell test) or specific EBV . iii. Mild elevation of liver enzymes in 50% Differential Diagnosis: Infectious mononucleosis-like illnesses may be caused by primary infection with , T. gondii, adenovirus, , HIV, or possibly rubella virus. Treatment: Rest and symptomatic treatments are the mainstays of management. Short courses of prednisolone 1mg/kg/day (<2 wk) may be helpful for complications of infectious mononucleosis. Avoid trauma to spleen. Complications: a. Subcapsular splenic hemorrhage or splenic rupture. b. Airway obstruction due to tonsillar enlargement. c. Alice in Wonderland syndrome : CNS affected leading to seeing things in abnormal sizes & shapes. d. e. Other CNS problems :, facial nerve palsy, transverse , and encephalitis. f. Occasional persistence of fatigue for a few years.

4 Prognosis : excellent if no complications. Kala-azar (visceral leishmaniasis) Etiology : Leishmania donovani & infantum parasites. Epidemiology :  The leishmaniases are estimated to affect 10–50 million people in endemic tropical and subtropical regions.  The parasite is dimorphic, existing as a flagellate promastigote in the insect vector and as an aflagellate amastigote that resides and replicates only within mononuclear phagocytes of the vertebrate host.  It typically affects children. Transmission : It is transmitted by phlebotomine sandflies with inoculation of human during a blood meal. Pathology & Pathogenesis : After bite they invade macrophage & replicate inside & and eventually rupture the cell and go on to infect other macrophages & then through lymph & blood to the organs. Thus, there is prominent reticuloendothelial cell hyperplasia in the liver, spleen, bone marrow, and lymph nodes. Clinical picture :  child may have a completely asymptomatic infection or an oligosymptomatic illness that either resolves spontaneously or evolves into active kala-azar.  mild constitutional symptoms (malaise, intermittent diarrhea, poor activity tolerance) and intermittent fever occur in oligosymptomatic & most recover but a few develop kala-azar 2-8 months later.  Active kala azar present with constitutional symptoms, , gross wasting, , jaundice, edema, and ascites & without treatment death may occur.

5  A small percentage of patients previously treated for VL develop diffuse skin lesions, a condition known as post-kala- azar dermal leishmaniasis. Diagnosis & investigations : 1. anemia , & leukopenia 2. elevated hepatic transaminase levels 3. hyperglobulinemia 4. Serologic testing by enzyme immunoassay, indirect fluorescence assay, or direct agglutination. 5. ELISA for K39 is very sensitive & specific. 6. smears or cultures of material from splenic, bone marrow, or lymph node aspirations are diagnostic. Differential Diagnosis : Malaria, typhoid fever, miliary tuberculosis, schistosomiasis, brucellosis, amebic liver abscess, infectious mononucleosis, and . Treatment:  Pentavalent antimony compounds (sodium stibogluconate [Pentostam]) are the mainstay of Rx.  Amphotericin B and the amphotericin lipid formulations are very useful in the treatment.  Interferon-γ & paromomycin are adjunctive dugs. Prevention: Avoidance of exposure to the sandflies.

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