GENERAL PRACTITIONER EXAM KIT-31

Explanation:

Scarlet fever is an illness that brings on a rash covering most of the body, a strawberry-like appearance of the tongue and usually a high fever. The most common source of scarlet fever is one form of a common bacterial infection known as strep throat.
Common symptoms are: Red rash that looks like a sunburn and feels like sandpaper, strawberry-like red and bumpy appearance of the tongue. Fever of 101 degrees Fahrenheit or higher, often with chills. Very sore and red throat sometimes with white or yellowish patches. Enlarged glands in the neck (lymph nodes) that are tender.
A bacterium called Streptococcus pyogenes, or group A beta-hemolytic streptococcus causes scarlet fever. Throat culture remains the criterion standard for confirmation of group A streptococcal upper respiratory infection.
Streptococcal antibody tests are used to confirm previous group A streptococcal infection. The most commonly available streptococcal antibody test is the Antistreptolysin O test (ASO). Currently, streptococcal antibody tests are not indicated during acute illness. Possible complications include rheumatoid fever, and poststreptococcal glomerulonephritis. Treatment is with antibiotics such as penicillin and amoxicillin.

Explanation:

Shigellosis is infection with species of the gram-negative bacillus Shigella, which results in dysentery that is characterized by frequent watery stools, often with mucus and blood, pain, fever, and dehydration.
Fever is frequently present and may reach 106˚F. Some children develop seizures. It is not known if these seizures occur simply from the high fever or as a specific complication of shigellosis.

Explanation:

Pneumococcal 7-valent vaccine produces a satisfactory immune response in a 1 year old, while polyvalent vaccine does not cause a good antibody response in children under the age of 2. Neither vaccine is available orally, nor is cost not a factor. The 7-valent vaccine requires multiple doses. Neither vaccine can be combined with MMR.

Explanation:

Rotavirus is the most common agent responsible for infantile diarrhea throughout the world in contrast to Vibrio. In tropical climates, rotavirus is the etiologic agent in 15%-50% of cases of acute diarrhea in children, and in temperate climates it accounts for 35%-60% of cases. Cytomegaolvirus has been shown to infect the colon on occasion. Bacterial pathogens account for 10%-15% of cases of acute childhood diarrhea: the most commonly identified bacterial pathogens in North American children are Campylobacter jejuni and various strains of salmonella and Shigella species. Some strains of Escherichia coli are pathogenic, causing sporadic cases of acute enteritis, epidemic diarrhea, and traveler´s diarrhea.

Explanation:

There are four combination vaccines used to prevent diphtheria, tetanus and pertussis: DTaP, Tdap, DT, and Td. Two of these (DTaP and DT) are given top children younger than 7 years of age, and two (Tdap and Td) are given to older children and adults. Children should get 5 doses of DTaP, one dose at each of the following ages: 2, 4, 6, and 15-18 month´s andr4-6 years. DT does not contain pertussis and is used as a substitute for DTaP for children who cannot tolerate pertussis vaccine. Td is a tetanus-diphtheria vaccine given to adolescents and adults as a booster shot every 10 years, or after an exposure to tetanus under some circumstances. Tdap is similar to Td but also containing protection against pertussis. A single dose of Tdap is recommended for adolescents 11 or 12 years of age, or in place of one Td booster in older adolescents and adults age 19 through 64.

Explanation:

Measles is a highly contagious, viral infection that is most common in children. It is characterized by fever, cough, coryza, conjunctivitis, enanthem (Koplik´s spots) on the buccal or labial mucosa, and a maculopapular rash that spreads cephalocaudally. Diagnosis is usually clinical. Treatment is supportive. Vaccination is highly effective.

Explanation:

Chlamydial genital infection is reported in 5%-30% of pregnant women, with vertical transmission to >50% of their infants at birth. An infant born to a mother with active chlamydial infection has a 50%-70% risk of acquiring infection at any anatomical site. Approximately 30%-50% of infants born to Chlamydia-positive mothers will develop conjunctivitis, and at least 50% these children will also have nasopharyngeal infection. Infants born to women with chlamydial infection may also develop associated pneumonia, but this affects only 10%-20% of this population.

Explanation:

Osteomyelitis is a pyogenic infection of the bone. The pathogenesis of the disease is similar to septic arthritis, with the origin of infection occurring from hematogenous spread, direct extension of a local infection, or direct inoculation of bone either from trauma (e. g. puncture wound or open fracture) or surgical manipulation. In children, the most frequent presentation is acute hematogenous spread. The most common location of osteomyelitis is the metaphysis of the distal femur and proximal tibia. The most prevalent pathogens are the same as those seen in septic arthritis. Staphylococcus aureus is the most common pathogen, with group A beta-hemolytic streptococci a distant second. Neonates are at risk for group B beta-hemolytic streptococci.
Patients with sickle cell disease are at risk for infection by Salmonella and other gram-negative bacteria, and patients in the 18- to 48-month age range are at increased risk for acute recurrent Salmonella osteomyelitis. Salmonella osteomyelitis frequently involves multiple sites and creates punched-out destructive lesions of the metaphysis and diaphysis. However even in patients with sickle cell disease, Staphylococcus aureus is still the most common pathogen for osteomyelitis.

Explanation:

Erythema infections m (fifth disease, parvovirus B19 infection) is a contagious viral infection that causes a blotchy or raised red rash with mild illness. Erythema infectiosum is caused by human parvovirus B19 and occurs most often during the spring months, often in geographically limited outbreaks among children and adolescents. Infection is spread mainly by breathing in small droplets that have been breathed out by an infected person. The infection can also be transmitted from mother to fetus during pregnancy, rarely resulting in stillbirth or severe anemia and excess fluid and swelling (edema) in the fetus (hydrops fetalis).
Symptoms begin about 4 to 14 days after infection but many children have none. However, some have a low fever and feel mildly ill for a few days. Seven to 10 days later, children develop red cheeks that often look like they have been slapped as well as a rash, especially on the (arms, legs, and trunk but not usually on the palms or soles. The rash [can be itchy and consists of raised, blotchy red areas and lacy patterns, particularly on areas of the arms not covered by clothing, because the rash may be worsened by exposure to sunlight.

Explanation:

Staphylococcal scalded skin syndrome is an acute epidermolysis caused by a staphylococcal toxin. Newborns and children are most susceptible. Symptoms are widespread bullae with epidermal sloughing.
The initial lesion is usually superficial and crusted. Within 24 h, the surrounding skin becomes painful and scarlet, changes that-quickly spread to other areas. The skin may be exquisitely tender and have a wrinkled tissue paper-like consistency. Large, flaccid blisters arise on the erythematous skin and quickly break to produce erosions. Intact blisters extend laterally with gentle pressure (Nikolsky´s sign). The epidermis may peel easily, often in large sheets. Widespread desquamation occurs within 36 to 72 h, and patients become very ill with systemic manifestations (eg, malaise, chills, fever). Desquamated areas appear scalded. Loss of the protective skin barrier can lead to sepsis and to fluid and electrolyte imbalance.
Diagnosis is by examination and sometimes biopsy. Treatment is antistaphylococcal antibiotics and local care. Prognosis is excellent with timely treatment.

Explanation:

Measles present classically with Koplik´s spots accompanied by conjunctivitis, photophobia, coryza, fever, and cough. The diagnosis of measles infection is primarily clinical. However, owing to the widespread administration of a live attenuated measles virus vaccine, the frequency of the disease has been reduced to virtually nil.

Explanation:

Explanation:

Erythema infectiosum with polyarthralgias is typical of parvovirus B19 infection in children. Juvenile rheumatoid arthritis is not associated with this skin rash. This rash is also not associated with Borrelia burdorferi (the causative agent of Lyme disease) or hepatitis B. Haemophilus influenzae is not typically associated with either polyarthralgias or erythema infectiosum.

Explanation:

Kawasaki´s disease is common in children. It is a mucocutaneous lymph node syndrome associated with coronary artery aneuryms, leading to myocardial infractions one to two percent of the time. The scarletiniform and morbilliform rash is common. Toxic shock syndrome is caused by staphyloooccus aureus and is associated with tampon use and post surgical infection. Scarlet fever presents in a similar way, however, as well as conjunctivitis, would be unusual. Streptococcus is the offending organism involved. Chicken pox would be a vesicular rash initially, and then become crusty. It is caused by Varicella Zoster virus, which is morphologically identical to, yet antigenically different from, other herpes viruses. A viral exanthem would be more confluent and diffuse. It would not be associated with a scarlet tongue.

Explanation:

The child presented to her general practitioner with the characteristic signs and symptoms of whooping cough: upper respiratory tract symptoms with the development of paroxysmal coughing, marked by episodes of coughing with an inspiratory and noisy “whoop” sound. Whooping cough is one of the most common vaccine- preventable disease among children. Despite the widespread use of vaccines, the disease has made a comeback in recent years. This child is at risk for whooping cough because she did not receive the DTP/DTaP vaccination and was exposed to a symptomatic adult. (Adults with a mild respiratory illness that is unrecognized as pertussis infections are frequently the source of infection. Immunization with DTP/DTaP would most likely have prevented the child´s infection with Bordetella pertussis (the causative agent of whooping cough).
Whooping cough has three stages. Stage 1 (catarrhal) begins with insidious, catarrhal upper respiratory tract symptoms (rhinitis, sneezing, irritative cough) that last 1-3 weeks. Stage 2 (paroxysmal) is marked by a paroxysmal cough characterized by 10-30 forceful coughs and ending in a loud inspiratory “whoop”. Vomiting commonly follows a paroxysm. Cyanosis, sweating, and exhaustion often accompany the coughing. This stage often lasts 2-4 weeks, with gradual improvement in stage 3 (convalescence), the patient experiences an irritative, chronic cough that may persist for several weeks or even months.
Antiviral drugs or use of bronchodilators would not have prevented the child´s infection with B. pertussis. Smoking in the home has been linked to chronic cough, asthma, and respiratory infections in children. However, smoking is not the cause of this child´s condition, and reducing smoking in the home would not have prevented whooping cough. Parents should however, still be advised to cease smoking or, at the very least, smoke outdoors and away from children.
Erythromycin for 14 days is the treatment for whooping cough if suspected or confirmed.

Explanation:

Explanation:

Explanation:

Epiglottitis is the most common disease of the upper respiratory tract produced by Haemophilus influenzae type B, a gram negative encapsulated rod. It is also common cause of otitis media in children and may cause bronchitis bronchiolitis, and pneumonia in adults. The incidence of serious disease caused by H. influenzae type B has decreased greatly with the introduction clan effective vaccine. The vaccine is composed of the polyribitol phosphate capsular polysaccharides coupled to a protein carrier molecule (diphtheria toxoid), given to children between 2 and 15 months of age. The purpose of conjugating the polysaccharide to protein is to stimulate TH2 cells to create the cytokines that will stimulate B cells to switch is of types of antibody. Without T-cell help, B lymphocytes can only make IgM, and IgM is not the best immunoglobulin for protection from a mucosal surface pathogen such as H. influenzae. This patient had not received the HiB conjugate vaccine and therefore was susceptible to this organism. Endotoxin is a component of the outer membranes of all gram-negative bacteria. H. influenzae possesses endotoxin, but it is not included in the vaccine because the molecule is not strongly immunogenic. Hemagglutinin molecules are used by both bacteria and viruses for adherence to host cells, however this is not present in the HiB vaccine. Mycolic acid is present in the cell wall region of acid-fast bacteria. H. influenzae does not possess mycolic acids and these molecules are not present in the HiB vaccine. Polyribitol phosphate is the capsular material of Haemophilus influenzae that is conjugated to the diphtheria toxoid. The role of the capsular polysaccharide is to serve as a hapten to which B lymphocytes will respond by producing antibody. However, in the absence of a conjugated protein, the only antibody isotype that would be made is IgM.

Explanation:

Explanation:

This patient has a patent ductus arteriosus, which results from failure of closure of the ductus arteriosus postnatally. This results in blood flowing from the aorta to the pulmonary artery. Patent ductus arteriosus is twice as common in girls. It is also associated with maternal rubella infection and with prematurity. Patent ductus arteriosus can be beneficial in providing pulmonary blood flow when there is an associated right ventricular outflow tract obstruction, or in supplying systemic flow in coarctation of the aorta. A small patent ductus arteriosus presents no symptoms.
Large patent ductus arteriosus can cause heart failure similar to large ventricular septal defects. Large patent ductus arteriosus causes a wide pulse pressure and bounding arterial pulses. An apical heave may be observed, in addition to a thrill at the second left intercostal space. The characteristic murmur is described s a “machinery” or to- and-fro, murmur heard in both systole and diastole. It can be less prominent or not heard in diastole in infants or in the presence of increased pulmonary vascular resistance. Chest radiographs show prominent pulmonary artery and increased pulmonary vascular markings.
Heart size may be normal or slightly enlarged. Echocardiography demonstrates the patent ductus arteriosus with its abnormal flow and a hyperdynamic left ventricle. Patent ductus arteriosus in premature infants may close spontaneously or respond well to indomethacin. It rarely closes spontaneously alter infancy, and surgical or catheter closure is recommended. Complications include congestive heart failure and infective endocarditis.
Early intrauterine herpes simplex virus infection with disturbance of embryogenesis occurs during the first 8 weeks of gestation. It may result in abortion, cutaneous scarring, or the following severe congenital malformations: intrauterine growth retardation, severe brain damage intracranial calcification, microcephaly, hydranencephaly, microphthalmia, chorioretinitis, retinal dysplasia, and short digits. Patent ductus arteriosus is not a typical malformation in this syndrome. Human papilloma virus is not a known cause of congenital malformations in newborns. Infection with these viruses may, however occur during birth by passage through an infected birth canal, and these babies are at risk of developing laryngeal papillomatosis or cutaneous/genital warts during the first 2 years of life.
Congenital syphilis develops when a fetus becomes infected with the spirochete Treponeme pallidum sometime after the 16th week of pregnancy. It can clinically be divided into early congenital syphilis (appearing before age 2) and late congenital syphilis (appearing alter age 2). The manifestations of early congenital syphilis are generally infectious (rhinitis, maculopapular exanthem, lymphadenopathy, hepatosplenomegaly, osteochondritis) and, since there is no primary stage, may resemble those of acquired secondary syphilis, but are more widely distributed, more severe, and last longer. The lesions of late congenital syphilis are either a hypersensitivity reaction of the host or scars and deformities resulting from the infection. Congenital varicella zoster syndrome (choice E) is caused by in utero infection of the fetus by varicella zoster virus during an episode of maternal varicella. It manifests with low birth weight congenital eye defects (microphthalmia, cataracts, and chorioretinitis);
encephalomyelitis, often with severe brain damage; hypoplastic limbs with flexion contractures; cutaneous scars; micrognathia; pneumonitis; and increased susceptibility to infection. Cardiac abnormalities are not a prominent lecture of this syndrome.

Explanation:

Explanation:

Measles (rubeola) is a very contagious, exanthematous respiratory disease with a pathognomonic enanthem. A live attenuated measles vaccine became available in 1963 in the U.S. and elsewhere, and measles is now an unusual disease in countries where this vaccine is widely used. However, measles continues to occur sporadically in mini-epidemics.
The measles virus is transmitted by respiratory secretions, predominantly through exposure to aerosols but also through direct contact with larger droplets. Patients are contagious for 1-2 days before the onset of symptoms until, 4 days after the appearance of the rash. Measles begins with a few-day respiratory prodrome of malaise, cough, coryza, conjunctivitis, nasal discharge, and increasing fever.
Just before the onset of the rash, Koplik´s spots appear as 1-to 2-mm blue-white spots on a bright red background shown as follows:

The characteristic erythematous, non-pruritic, maculopapular rash of measles begins at the hairline and behind the ears, spreads down the trunk and limbs to include the palms and soles, and often becomes confluent. At this time, the patient is at the most severe point of the illness. By the 4th day, the rash begins to fade in the order in which it appeared. Brownish discoloration of the skin and desquamation may occur later. Fever usually resolves by the 4th or 5th day after the onset of rash; prolonged fever suggests a complication of measles. Lymphadenopathy, diarrhea, vomiting, and splenomegaly are common features. Therapy for measles is largely supportive and symptom based.
Erythema infectiosum, or Fifth´s disease, is a mild illness caused by parvovirus B-19. It usually begins as a marked erythema of the cheeks, giving a “slapped cheek´ appearance.
Hand-foot-mouth disease presents with a prodrome of fever and anorexia, followed by ulcers on the tongue and oral mucosa and a vesicular rash on the hands and feet. Roseola infantum presents with an abrupt onset of a high fever, with temperatures up to 39.5 °C-41.1 °C (103-106°F). A maculopapular rash appears on the trunk on the 3rd or 4th day when the fever breaks.
Rubella causes a mild syndrome, which is characterized by an erythematous, maculopapular, discrete rash, generalized lymphadenopathy, and fever. It can cause congenital rubella syndrome in the infant if the pregnant mother is infected with the virus.

Explanation:

Rocky Mountain spotted fever is a rickettsial disease characterized by fever, headache, and a rash. It is caused by Rickettsia rickettsii the vector a tick, and the reservoir rodents and mammals. Clinically, the onset is nonspecific. The patient may complain of fever, myalgias, nausea, and vomiting. The typical triad of the illness is headache, fever, and a rose-colored, blanching, maculopapular rash that begins on the extremities and spreads centripetally to the entire body. The erythematous macules soon turn into petechiae as the result of vasculitis. Diagnosis is established based on history and physical examination. Early in the disease, there is no single laboratory´ study to confirm the diagnosis, but in the convalescent phase, serology may be confirmatory. Thrombocytopenia, a low leukocyte count, and low serum sodium aid in making the diagnosis.
Treatment should be initiated on clinical diagnosis alone as early as possible. Tetracycline or doxycycline is the antibiotic of choice.
These may be given even to patients younger than 8 years of age, because it is a potentially fatal disease (10% mortality); tooth discoloration and growth delay are dose-dependent and it is unlikely that the patient will need multiple courses of the drug.
Amoxicillin is the treatment of choice for Borrelia burgdorferi infection (Lyme disease) in children younger than 8 years of age. In adults, doxycycline is also recommended for Lyme disease. It is not active against Rickettsia rickettsii because it is an intracellular organism that dots not have a cell wall to destroy.
Amoxicillin/clavulanate is not active against Rickettsia rickettsii for the same reason as amoxicillin alone. Adding a beta- lactamase inhibitor would not change the spectrum to cover rickettsia infections.
Ceftriaxone is the treatment of choice for the secondary manifestations of Lyme disease, such as neurologic and cardiac involvement. It is not active against Rickettsia rickettsii for the same reason as the other cell-wall synthesis inhibitor antibiotics.
In patients not able to take tetracyclines, chloramphenicol should be considered, but because of its side-effect profile, it is a second-line option. Potential adverse effects of chloramphenicol include bone marrow suppression, plastic anemia, leukemia and Gray baby syndrome.
Penicillin G is the treatment of choice for congenital and tertiary syphilis. It has no activity against rickettsial infections because of its mechanism of action.

Explanation:

This boy most likely has hepatitis A. Although it is more common in developing countries, it is still a common infection in the developed world. It is transmitted by the fecal-oral route when contaminated food or water is congested. The incubation period is about l5-40 day. Ninety percent of children acutely infected with hepatitis A are asymptomatic. The virus is shed in the feces 2-3 weeks before the onset of jaundice until approximately l week after onset. Most infected children are infectious for a long time before they are symptomatic. Therefore, hepatitis A is very difficult to control. Large outbreaks frequently occur in daycare centers. Diagnosis is best made by determination of IgM levels against hepatitis A virus.
The presence of IgM for hepatitis A suggests acute infection; this antibody peaks at 4-6 weeks and does not persist beyond 6 months. IgM is produced in the primary infection, but for most viral infections, including hepatitis A, it persists for a life time. Therefore, the presence of IgM against hepatitis A could mean a previous infection and is not diagnostic of a current infection. Stool culture for hepatitis A cannot be used to confirm the diagnosis.
Prophylaxis with immunoglobulin is recommended for the household and close contacts of the infected person within the first 2 weeks of exposure. Strict hand washing is also very important. There is a killed-virus vaccine available that provides immunity to travelers to developing countries if given in two doses 6-12 months apart.
The presence of hepatitis B surface antigen in the serum signifies an active/current infection with hepatitis B. IgG against hepatitis B surface antigen comes from an immunologic response to either the hepatitis B virus surface antigen from an infection, or from the hepatitis B virus vaccine.

Explanation:

Explanation:

These children most likely have erythema infectiosum, which is caused by parvovirus B19. It is a benign, sell- limited infection characterized by mild systemic symptoms and rash. The typical rash is lace-like on the trunk and proximal extremities and there is often a facial rash that gives the patient an intensely red, “slapped cheek´ appearance. In general, the treatment is supportive care only. Intravenous immunoglobulin therapy may be considered for immunocompromised patients.
Scarlet fever, caused by group a beta-hemolytic streptococci is characterized by fever, chills, headache, sore throat and sandpaper- like rash. Patients often have a “strawberry tongue,” circumoral pallor, Pastia lines, and inflamed tonsils. Desquamation of the rash may occur. Penicillin is the drug of choice.
Human herpesvirus 6 causes exanthem subitum (roseola). It is characterized by a high fever (not exceeding 41 °C [106 °F]) that lasts for 3 to 4 days with minimal physical findings. The fever resolves on the third or fourth day, and a maculopapular rash appears on the trunks, arms, neck, and face. Occipital lymphadenopathy may occur.
Treatment includes supportive therapy with antipyretics and fluids. Measles, caused by the measles virus, is characterized by a high fever, maculopapular rash, cough, coryza, conjunctivitis, and Koplik spots on the buccal mucosa. Treatment is supportive. Mumps, caused by the mumps virus, is characterized by fever headache, muscle pain and malaise. The prodrome is usually followed by ` pain and swelling of the parotid gland. Treatment is supportive.
Rubella caused by the rubella virus, is characterized by a rash and enlargement and tenderness of the post occipital, retroauricular, and cervical lymph nodes. Patients may also have pharyngitis, a low-grade fever, and upper respiratory infection symptoms. Treatment is supportive.

Explanation:

The diagnosis is atopic eczema. It is associated with elevated IgE levels and almost all affected children will develop allergic rhinitis and/or asthma. It typically begins during infancy, almost all by age 5 years. The skin is very reactive and pruritic, especially at night, and it is the scratching that leads to the characteristic skin lesions. Many factors such as foods, inhalants, and changes in humidity, infection, and irritants may exacerbate the pruritus. The initial lesions are erythematous papules with excoriation and serous exudate. Overtime, the disease becomes subacute with the presence of scaling papules. The chronic form is characterized by lichenification. The underlying problem is dry skin (xerosis), especially in winter. In infancy, the face, scalp, and extensor surfaces of the extremities are generally involved. With chronicity, the disease is localized to the flexural folds of the extremities and usually goes into remission. At this point the skin is pruritic and becomes inflamed with irritant exposure. The mainstay of treatment is appropriate skin hydration. Hydration by lukewarm, soaking baths, followed by the application of an emollient, allows for retention of moisture and provides symptomatic relief.
Antihistamines generally do not provide much benefit because histamine is only one of many mediators that can induce skin pruritus. The best use of the older antihistamines, such as diphenhydramine, is to help with sleep at night when the pruritus is usually worse.
Phototherapy is an adjunct in the treatment of atopic dermatitis. It has immunosuppressive effects and is indicated in patients with severe, widespread disease. Side effects include erythema, pain, pigmentation, and predisposition to malignancy.
The goal of therapy is to use the emollients for skin hydration and low-potency topical glucocorticoids for maintenance. A higher-potency topical steroid class may be used for short periods if there is an acute, more severe flare-up. Steroids should not be used on the face or intertriginous areas because of the formation of striae and skin atrophy.
Topical immunomodulators such as tacrolimus, inhibit the activation of a number of key cells in atopic dermatitis. The ointment is safe and effective in children and may be used safely on the face. It does not produce skin atrophy. The lesser concentration is approved for short-term and intermittent long-term use in children 2 to 15 years of age, and the higher concentration for children at least 16 years of age.
Coal-tar preparations are anti-inflammatory and antipruritic, but they are not as effective as the topical steroids or immunomodulators. Coal-tar preparations are most useful in decreasing the potency of a topical steroid being used in chronic atopic dermatitis. The common side effects are photosensitivity, folliculitis, and irritation.
mmon side effects are photosensitivity, folliculitis, and irritation.

Explanation:

This patient has streptococcal pharyngitis. The most common bacterial cause is group A beta-hemolytic streptococci- Rapid Strep antigen kits have a high degree of sensitivity and specificity. The gold standard is throat culture and it should be performed in all clinically suspicious cases. Routine blood work will reveal an elevated erythrocyte sedimentation rate, left shift of the differential white blood cell count and an increased number of polymorphonuclear leukocytes and band forms. Treatment of viral pharyngitis is symptomatic, whereas bacterial cases are treated with antibiotics. Penicillin is the antibiotic of choice and amoxicillin an acceptable alternative. Complications of streptococcal pharyngitis include rheumatic fever, glomerulonephritis, peritonsillar abscess, and retropharyngeal abscess. All but glomerulonephritis are preventable with early antibiotic treatment Pathogenesis of poststreptococcal glomerulonephritis seems to be immunologically mediated, and the incidence varies with the prevalence of nephritogenic strains in the community. The latent period between streptococcal pharyngitis and glomerulonephritis is 1 to 2 weeks.
A peritonsillar abscess should be suspected when a patient with strep pharyngitis has persistent fever and an increasingly severely sore throat. The patient drools, and the affected tonsil bulges medially. The uvula will deviate to the noninvolved site and the patient has a “hot potato” voice. Intravenous antibiotics and surgical drainage are the treatment.
Retropharyngeal abscess presents as a soft tissue mass in the lateral neck of a patient with history of recent pharyngitis. Lateral films of the neck confirm the diagnosis. Intravenous antibiotics and surgical drainage are the treatment.
Rheumatic fever is a complication of group A streptococci infection that presents as carditis and chorea in a patient with an elevated antistreptolysin C titer and a past history of untreated or inadequately treated upper respiratory tract infection.
Scarlet fever is most often the result of pyrogenic exotoxins produced by beta-hemolytic group A streptococci. Fever and sore throat precede the skin eruption by several days. The rash begins on the face and neck and spreads downward, sparing palms, soles, and the perioral area (circumoral pallor). Tiny, scaly papules appear on the trunk, giving the skin the texture of sandpaper. Fine desquamation ensues from the face and neck down whereas palms and soles often desquamate in a “gloves and socks” fashion. The erythema is accentuated in skin folds, where petechiae may also occur. The most characteristic mucosal lesion is the strawberry tongue: protruding, enlarged, g erythematous papillae and a thick white coating. A diagnosis of scarlet fever may be made clinically and is supported by throat cultures and a rising antistreptolysin O titer.

Explanation:

The clinical presentation is consistent with diaper dermatitis. The most important clinical clue is the distribution of the erythematous areas. The usual cause of diaper dermatitis is irritant contact dermatitis, resulting from the concomitant action of fecal and urinary enzymes, entrapped moisture and excessive heat in the diaper area. Avoiding tight occlusion by diapers, bathing with mild soaps and water, and frequent diaper changes constitute the essential approach to treatment. In the most severe cases, topical application of low-strength corticosteroid cream and/or zinc oxide may be indicated.
Candidiasis manifests with papules and plaques rather than extensive shiny areas of erythema. Candida infection, however, develops superimposed on diaper dermatitis. If signs of candidiasis are present a topical antifungal agent should be used in treatment.
Langerhans cell histiocytosis is a severe disease due to neoplastic proliferation of Langerhans cells. In infants, the condition manifests in its systemic life-threatening form known as Letterer-Siwe syndrome. The baby is critically ill, with fever and a diffuse scaly rash.
Psoriasis may be confused with diaper dermatitis. Psoriasis is characterized by well-demarcated silvery plaques that often involve skin folds in infants.
Seborrheic dermatitis manifests with sa1mon-colored, scaly, oily plaques that may affect the-diaper area, but most commonly involve the scalp and face.

Explanation:

This question is essentially asking the reader to diagnose the condition in the mother that would lead to the development of the signs and symptoms in the child. Then the reader must determine what the treatment of choice is for the mother´s infectious condition. TORCH is an acronym referring to a group of microorganisms that lead to specific pathologic changes that occur during fetal or neonatal infection. The T stands for toxoplasma, the O for others, the R for rubella, the C for cytomegalovirus, and H for herpes simplexvirus. The “others” portion of acronym TORCH include syphilis and tuberculosis as well as a few other less common microorganisms. Pathologic manifestations of the TORCH complex include brain lesions (encephalitis and intracranial calcifications), ocular manifestations (chorioretinitis), and a variety of cardiac abnormalities. The organism Treponema pallidum causes both adult and congenital syphilis. Congenital syphilis may result in the development of typical TORCH pathologic changes as well as the following: saddle nose (flattening of the nose), Hutchinson´s teeth (notched incisors), mulberry molars (deformed molars), saber shins (outward bowing of the anterior tibias) and interstitial keratitis (vascularization of the cornea). The combination of deafness, interstitial keratitis, and notched incisors is known as Hutchinson´s triad. The treatment of choice for syphilis is consecutive daily intramuscular injections with procaine penicillin. The actual dosage and duration for the therapy are determined by the patient´s clinical presentation (chancre, secondary mucocutaneous manifestations, neurosyphilis, etc.). If no clinical staging is possible (as is usually the case), serologic staging determines the treatment regime. If the patient is allergic to penicillin, other treatment options exist, such as doxycycline. Acyclovir is used in the treatment of herpes infections.
Ciprofloxacin is used in the treatment of a variety of gram negative infections. Ganciclovir is used in the treatment of cytomegalovirus infections. Isoniazid and rifampin are the drugs of choice for the treatment of typical, drug sensitive tuberculosis.

Explanation:

BCG vaccine may be given to newborns at high risk of exposure.
The BCG vaccine is an attenuated strain; it provides approximately 70% protection.
It should not be given to these children. A low reactivity Heaf test (grade 0-1) should be documented before administration.
BCG is given at comprehensive school entry (age 11-13).
It has also found a use in stimulating the immune system for the treatment of some cancers

Explanation:

Seborrhoeic dermatitis primarily affects the scalp and intertriginous areas. It is most common in the first 6 weeks of life, but can occur in children up to 12 months of age. Involvement of the scalp is frequently termed “cradle cap”, and manifests as greasy, yellow plaques on the scalp. Other commonly affected areas include the forehead and eyebrows (as in the photo), nasolabial folds, and external ears. Involvement of skin creases, such as the nappy areas, can lead to secondary Candidal infection and maceration. The etiology is unknown. Treatment includes the use of a mild tar shampoo, oatmeal baths, and avoidance of soaps. Occasionally, a mild topical steroid may be indicated.

Explanation:

Cat-scratch disease is infection caused by Bartonella henselae.
Symptoms are a local papule and regional lymphadenitis. Within 3 to 10 days after a scratch, most patients develop an erythematous, crusted papule (rarely, a pustule) at the scratch site. Regional lymphadenopathy develops within 2 weeks. The nodes are initially firm and tender, later becoming fluctuant, and may drain with fistula formation. Fever, malaise, headache, and anorexia may accompany lymphadenopathy. Treatment is local heat application and analgesics. If a lymph node is fluctuant, needle aspiration usually relieves the pain. Antibiotic treatment is not clearly beneficial and generally should not be given for localized infection.

Explanation:

With widespread immunizaton against Haemophilus influenzae infection, Streptococcus pneumoniae has become the, predominant cause of serious bacterial infection in infants and young children. In a study of about 9000 well-appearing older infants and young children, 149 (7%) had positive blood cultures, 92% of which were S. pneumoniae.

Explanation:

Explanation:

Cytomegalovirus (CMV) is the most common congenital infection and occurs in up to 2% of newborns. It is the leading cause of congenital hearing loss. The virus is transmitted by contact with infected blood, urine, or saliva, or by sexual contact. Risk factors for CMV include low socioeconomic status, birth outside North America, first pregnancy prior to age 15, a history of cervical dysplasia, and a history of sexually transmitted diseases. Infection can be primary or a reactivation of a previous infection. While the greatest risk of infection is during the third trimester, those occurring in the first trimester are the most dangerous to the fetus.

Explanation:

Croup is acute inflammation of the upper and lower respiratory tracts caused most com only by parainfluenza virus type 1 infection. It is characterized by a barking cough and inspiratory stridor. Diagnosis is usually obvious clinically but can be made by anteroposterior neck x- ray. Treatment is antipyretics, hydration, nebulized racemic epinephrine, and corticosteroids. Prognosis is excellent.

Explanation:

Gregg´s syndrome, or congenital rubella syndrome, manifests with four major abnormalities: 1) cataracts, 2) iris abnormalities, 3) glaucoma, and 4) retinopathy. Tooth abnormalities are seen in Hutchinson´s triad and are indicative of congenital syphilis.

Explanation:

At a two-month well-baby checkup, DTP (diphtheria and tetanus toxoids with pertussis), TOPV (oral attenuated poliovirus type 1, 2, and 3), and Hib (Haemophilus influenzae type b) vaccines are typically administered. DTP and Hib are administered at six months. DTP and TOPV are administered at 18 months and from four to six years. MMR and Hib are administered at the 15-month well-baby checkup. Finally MMR is administered to children at the age of 11- 12 years.

Explanation:

Staph aureus is by far the most common cause of joint sepsis in this age group. Group B strep is common in neonates and H. influenza in children six weeks to six years.

Explanation:

While ampicillin is often the drug of choice for the treatment of Haemophilus influenzae meningitis, rifampin is the drug of choice for prophylaxis. In fact, rifampin is used not only for the prophylaxis of Haemophilus influenzae meningitis, but also of Neisseria meningitides meningitis. Oxacillin is utilized for the treatment of Staphylococcus aureus meningitis. Penicillin is used for both Neisseria and Streptococcus Pneumoniae meningitis. Vancomycin is utilized in the treatment of methicillin-resistant Staphylococcus aureus meningitis. Listeria meningitis is treated with trimethoprim-sulfamethoxazole if penicillin or ampicillin fails.

Explanation:

Of the organisms listed, Escherichia coli is the most common cause of neonatal meningitis and sepsis. Group B Streptococci are also important causes. Haemophilus influenzae is the number one cause of epiglottitis, happening most frequently in children.

Explanation:

Pseudomonas aeruginosa is a Gram negative bacterium which is not common in neonatal meningitis. It can occur in debilitated patients and it carries a very high mortality. S. pneumoniae is more common in meningitis in adults (80% of cases) than in infants. H. influenzae is responsible for most cases of meningitis in children older than one month. Although vaccines might not be very effective in infants less than two months of age, it formerly caused 50% of the cases of bacterial meningitis in the U.S., but the wide- spread use of H. influenzae type B conjugate vaccine has dramatically reduced the number of cases. It is still a cause of mortality in infants. N. meningitidis is Gram negative diplococci, a cause of meningitis, and occurs most often in the first year of life. It is also a common cause of meningitis in closed populations, such as boarding schools and military barracks, especially among adolescents and young adults. Listeria monocytogenes strikes mainly immunocomprised patients, i.e., patients with renal failure, on steroid therapy, or with AIDS. This may include some neonates.

Explanation:

Explanation:

Explanation:

Explanation:

Poliovirus, which is a single stranded positive sense RNA virus is naked (i.e., non-enveloped) and hence will not be inactivated by lipid solvents such as ether. The live virus vaccine had colonized the intestinal tract of the infant and was still being shed 2 weeks after the earlier oral dose. This same virus, the vaccine strain, is likely to be found in sewage, as all vaccinated infants will shed virus for a period of time after immunization with oral polio vaccine (OPV).

Infection with adenovirus is not likely. Although several serotypes may cause diarrheal disease and are non-enveloped, they have a DNA genome.

Infection with hepadnavirus is not likely, although hepatitis B may cause diarrhea occasionally. It is a double stranded DNA virus. Infection with polio is not likely because mutations of the vaccine strain of the Sabin vaccine are very rare. It is possible, but not the most likely explanation for the present findings. Infection with rotavirus is not likely, although this is the major cause of diarrheal disease in infants under the age of 2 years. It is a member of the reovirus family and, as such, is double stranded. This virus causes hospitalization of 30 to 40% of the infected infants, and kills hundreds of thousands of infants in developing nations where access to hospitals is not readily available. Therapy for the watery diarrhea produced by this agent is fluid and electrolyte replacement.

Explanation:

This patient most likely has a complicated urinary tract infection caused by Proteus mirabilis or Ureaplasma urealyticum. Lomefloxacin is a fluoroquinolone antibiotic indicated for the treatment of a wide variety of infections caused by both gram- negative and gram-positive organisms. This agent is primarily used in the treatment of lower respiratory tract and urinary tract infections. Lomefloxacin and other fluoroquinolone antibiotics have been associated with the development of arthropathy, myalgias, and leg cramps when administered to children younger than 18 years of age. Azithromycin is a macrolide antibiotic that is generally well tolerated. The most common side effects of this agent are mild nausea and abdominal pain. Metronidazole is an antiprotozoal and antibacterial associated with the development of seizures and peripheral neuropathy. Furthermore, this agent can produce a disulfiram-like reaction when taken with alcohol. Rifampin is an agent used to treat all forms of tuberculosis. It is also used in asymptomatic carriers of Neisseria meningitidis. Rifampin is associated with the development of hepatotoxicity, hyperbilirubinemia, porphyria, and possibly cancer.
Tetracycline is an antibiotic known to cause photosensitivity, pseudotumor cerebri, and a variety of maculopapular rashes.

Explanation:

Explanation:

Explanation:

The diseases listed in this question are all vesiculobullous. Erythema multiforme (EM), Stevens-Johnson syndrome, and toxic epidermolysis all represent a spectrum of disorders. Stevens- Johnson syndrome is the correct diagnosis in the question. The lesions look like those of EM but involve the face, trunk, and extremities; they are more widespread; and there must be involvement of at least two mucosal surfaces (eyes, mouth, upper airway, gastrointestinal tract, or anogenital area). Skin tenderness is generally minimal, but pain from mucosal ulceration is severe. New lesions occur in crops over 4 to 6 weeks. The bullae and erosions may result in blood loss, fluid loss, and bacterial superinfection. Eye involvement may include anterior uveitis, corneal ulceration, and panophthalmitis. Ocular scarring and visual impairment may remain. Other complications would depend on which mucosal surfaces were involved. The most common infectious cause of Stevens-Johnson syndrome is Mycoplasma pneumoniae. There are many other causes, including herpes simplex, M. tuberculosis hepatitis B, Ebstein- Barr virus, enterovirus, and other infections. In addition, other noninfectious causes include leukemia and lymphoma; the antibiotics penicillin, sulfonamides, isoniazid, tetracyclines, cephalosporins, and quinolones; the anticonvulsants phenytoin, phenobarbital, carbamazepine, valproic acid, and lamotrigine; and other causes such as radiation, captopril, nonsteroidal anti-inflammatory drugs, sunlight, pregnancy, and allopurinol.
Erythema multiforme can present as erythematous macules, papules, vesicles, or bullae to areas of confluent erythema. It is most common between ages 10 and 30 years. It tends to burn and itch. The diagnosis is clinical: doughnut-shaped, target like papules with an erythematous outer border, an inner pale ring, and a purple necrotic center. Lesions usually appear abruptly and symmetrically on the extensor surfaces of the upper extremities. These lesions commonly expand outwardly. There may be oral lesions, but no other mucous membrane surfaces are involved and it does not develop into Stevens- Johnson syndrome. The lesions usually resolve within 2 weeks. Most cases are related to- herpes simplex infection. Treatment is supportive. Toxic epidermal necrolysis (TEN) is the most severe disease in this spectrum, involving extensive toxicity and necrolysis of the mucous membranes with more than 30% of the body surface area. It is thought to represent a hypersensitivity reaction involving the basal cell epidermal layer, and is triggered by the same factors as those for Stevens-Johnson syndrome. There is widespread blister formation with erythema and tenderness, absence of target lesions, sudden onset and spread within 48 hours, and full-thickness epidermal necrosis. As may be seen with staphylococcal scalded skin syndrome (SSS), the Nikolsky sign is present-denudation of the skin with gentle tangential pressure with TEN the skin denudes only in areas of erythema, whereas with SSS it will occur on any part of the skin. In addition, the mucous membrane involvement is not as severe as with EM.
Bullous pemphigoid is rare in children. In this illness, blisters (fluid-filled, of various sizes) arise in crops, mostly on the flexural aspects of the extremities, axillae, groin, and central abdomen. The base of the blister may be normal skin or may be erythematous, eczematous, or urticarial. Infants tend to present with facial involvement and involvement of the palms and soles. Pruritus and burning may be present but constitutional symptoms are not prominent Oral lesions are less severe than the disorders presented above. This is an autoantibody disorder, and IgG and C3 may be seen at the basement membrane by immunofluorescence. There is also an inflammatory infiltrate consisting mostly of eosinophils. Primary treatment is with topical corticosteroids.
Epidermolysis bullosa represents a wide variety of hereditary blistering disorders. Differences are seen histologically from the superficial skin to deep dermal areas. All are characterized by trauma-induced blistering and by blistering in warm weather. The simplex form is autosomal-dominant and is usually present from birth.
Bullae are seen most commonly on the hands, feet, elbows, knees, legs, and scalp. Lesions heal with the scarring. The other forms may be progressive and more extensive with mucosal involvement, and may lead to squamous cell carcinoma.

Explanation:

Erythema migrans develops 3 to 32 days after the bite of a deer tick (Ixodes scapularis) infected by Borrelia burgdorferi. The rash begins as a papule that expands to form an erythematous annular lesion with central clearing. It may be accompanied by malaise, lethargy, fever, and arthralgias.
Acrodermatitis chronica atrophicans is a late complication of Borrelia azelaic infection, seen mostly in Europe, in which the acral integument becomes atrophic and translucent. It may develop decades after the initial infection occurred.
Erythema ab igne is a reticulated brown network that develops on skin chronically exposed to high temperatures, such as i repeated applications of heating bottle to the same skin site or sitting close to radiator with heat directed toward the skin from a very short distance. It is permanent and may undergo malignant transformation to squamous cell carcinoma many years later.
Erythema annulare centrifugum is an inflammatory skin disease of unknown etiology that usually develops in adults in the form of erythematous annular plaques with central clearing and peripheral “trailing” scale. Some believe it is a reactive pattern seen as an id reaction to remote infectious foci, such as inflammatory tinea of the feet.
Erythema infectiosum, also called fifth disease, is a viral infection caused by human parvovirus B19. It is mildly contagious and affects children 3 to 12 years of age. First an erythematous malar rash appears, followed by an erythematous maculopapular eruption on the extensor extremities the next day. When the rash fades, a few days later, areas of central clearing leave behind a reticulated, lacy patterned rash that waxes and wanes for an average of 9 to 11 days.
Erythema Marginatum occurs in rheumatic fever.

Explanation:

The Jones Criteria for the diagnosis of rheumatic fever was revised in 1992 by the American Heart Association. The criteria are for the initial attack of rheumatic fever only, not for recurrences. There are five major criteria: carditis, migratory polyarthritis, erythema marginatum, subcutaneous nodules, and chorea.
The presence of any two with microbiologic or serologic evidence of a recent group A streptococcal infection is diagnostic. However, there are three circumstances in which the diagnosis may be made without strictly employing the Jones criteria: chorea as the only manifestation, indolent carditis, and recurrence of rheumatic fever.
There are two clinical minor criteria: arthralgia and fever. There are also two laboratory criteria elevated acute phase reactants and prolonged PR interval on electrocardiogram. The presence of one major and two minor criteria is diagnostic, but again, it needs to be supported by evidence of a recent group A streptococcal infection.
The patient here presents with erythema marginatum. It is a characteristic rash of rheumatic fever, but is rare. It consists of erythematous, serpiginous, macular lesions with pale centers that are not pruritic. The lesions occur primarily on the trunk and extremities but not the face. This is the only manifestation that is mentioned in the question, so we would need one more major or two minor criteria.
Thus, there is no single answer choice that would fulfill the criteria.
But that is not what the question asks. Ultimately, there has to be evidence of a recent streptococcal infection. This is an absolute requirement. This is what the question is asking.
Of the answer choices, the only one that will confirm a recent infection is the elevated anti-DNase B titer. Acute rheumatic fever typically follows a group A streptococcal infection by 2 to 4 weeks.
Many patients have no history of an antecedent pharyngitis; therefore, y evidence must be based on increasing serum anti streptococcal antibody titers. There are three different antibodies that are measured clinically: antistreptolysin O anti-DNase B, and antihyaluronidase.
Anti-DNase B is the most sensitive and specific, but 100% accuracy is approached if all three are measured. So when the diagnosis is suspected, multiple tests may need to be performed.
Arthralgia in itself does not need to present to ultimately confirm the diagnosis. The argument is the same for elevated erythrocyte sedimentation rate, fever and prolonged PR interval.

Explanation:

This boy has infectious mononucleosis, which is characterized by fever, adenopathy, splenomegaly, lymphocytosis with atypical lymphocytes, and evidence of acute infection by Epstein-Barr virus. Because this sore throat is confused with streptococcal sore throat, ampicillin is often initiated. This triggers the appearance of an immune complex-related rash. Treatment is symptomatic. Contact sports should be avoided for 2 to 3 weeks, or until splenomegaly has resolved.
Beta-hemolytic Group A streptococci is a common cause of acute purulent pharyngitis in children. Acute purulent pharyngitis presents with fever, chills, and a sore throat. The tonsils are erythematous, edematous, and covered with purulent exudates. A quick diagnosis may be made in the office by doing a rapid strep test supported by bacterial cultures if the test is negative. On the other hand, a positive strep test is enough to start antibiotic therapy.
Penicillin is the drug of choice.
Herpes simplex virus is the cause of oro labial and genital herpes. The initial episode is a painful vesicular eruption of the oropharynx or genitalia that resolves without treatment in l to 2 weeks. The virus remains latent in cranial or spinal ganglions and, in approximately 10% of patients, will continue to recur with certain triggering events. Herpes simplex infection does not cause hepatosplenomegaly or generalized) lymphadenopathy.
Human immunodeficiency virus infection is the cause of AIDS. Patients may present with lymphadenopathy, hepatosplenomegaly, parotitis, and recurrent or persistent upper respiratory tract infections. Later, candidiasis, chronic diarrhea, herpes zoster, and other opportunistic infections ensue as the lymphocyte counts drop.
Rubivirus is the cause of rubella (German measles), a viral infection characterized by a maculopapular exanthem and tender lymphadenopathy of the post occipital, retroauricular, and cervical lymph nodes. Forchheimer spots are rose spots seen on the soft palate that may precede the skin rash.

Explanation:

This family has scabies, an infestation caused by the mite Sarcoptes .scabiei, and the treatment of choice for the entire family is permethrin cream application overnight repeated once in 7 days. All family members and caretakers of the child should be treated. Bed linens and clothes should be laundered in hot water, or dry cleaned if laundering is not feasible.
Ivermectin) in a single oral dose is used to treat scabies in immunocompromised individuals who have overwhelming infestation that would not respond to standard topical therapy. It is not recommended for use in ordinary scabies.
Lindane cream should not be used in small infants because of its potential for neurotoxicity. It is relatively safe for use in adults, but permethrin cream has an established safety record that A makes it the treatment of choice today.
Scabies does not resolve spontaneously except in rare instances where the immune response is so strong that it eliminates the mite. Even if that were to happen, chances are that reinfestation would occur from other family members or caretakers, so treatment is necessary. It is very important to treat all family members and caretakers simultaneously for the same reason. Therefore, it is incorrect to say that no treatment is necessary because the disease will resolve spontaneously.
Precipitated sulfur in petrolatum was often used to treat scabies in infants and pregnant women but has become rather, obsolete; permethrin cream has proven to be just as safe and much easier to use.
Precipitated sulfur in petrolatum has an offensive “rotten-egg” odor that confines the treated person to the home for the duration of the treatment. In addition, it is applied daily for 7 days without bathing in the meantime. Permethrin cream is applied once to the entire skin, washed off 8 hours later, and reapplied in 7 days. It is by far more convenient and comfortable for the patient to use.

Explanation:

Explanation:

Messing with a dog while the dog is eating, and being bitten in response, is considered to be a provoked attack, and thus not indicative of aggressive behavior on the part of the dog. The bite is in the hand; therefore, there is plenty of time for the virus to travel in the direction of the brain, so that therapeutic measures would still be effective should the future behavior of the dog suggest that he is rabid.
Passive immunization, active immunization, or a combination of both is not required in this low-risk situation. Had the bite been in the face, an area where rabies is prevalent, a more aggressive approach would have been justified. Killing the animal and examining the brain is the norm for wild animals that are captured alive, since their behavior cannot be deemed to be “normal” or “abnormal. It is also the appropriate step if observation of a domestic animal by a veterinarian suggests that signs of rabies are developing in the animal.

Explanation:

This neonate is most likely suffering from listeriosis, caused by Listeria monocytogenes. It can be acquired by mothers, who are exposed to unpasteurized dairy products or raw vegetables, or those exposed to cattle or sheep manure, especially mothers who live on farms. Mothers who acquire Listeria may experience flulike illnesses, with headache, malaise, fever, nausea, vomiting, and generalized body aches. The bacteria have a predilection for causing amnionitis, which may then produce abortion, stillbirth, or neonatal sepsis. The presence of brown, murk, amniotic fluid may be a helpful diagnostic clue. Neonates present with a full-blown picture of neonatal sepsis, as indicated by respiratory distress (tachypnea, grunting, apnea, and retractions), temperature instability, poor feeding, and lethargy/irritability. Sometimes with severe infection, a characteristic disseminated disease in the fetus called granulomatosis infanti septicum (pathognomonic for listeriosis) can cause granuloma formation and tissue destruction in many tissues, including skin (papular or ulcerative nodules), liver, adrenal glands, lymphatic tissue, lungs, and brain. Early-onset neonatal listeriosis presents with sepsis with or without granulomatosis infantisepticum, whereas late-onset presents 2-3 weeks after birth with meningitis and sepsis.
However, blood and CSF culture confirms the diagnosis.
The microorganisms most commonly associated with early-onset sepsis include group B Streptococcus (GBS), Escherichia coli Haemophilus influenzae, and Listeria monocytogenes.
Congenital cytomegalovirus infection can cause asymptomatic (most commonly) to mild to severe disease in neonates. Some finding that clue you in to the diagnosis include small size for gestational age, hepatosplenomegaly, petechiae and purpura of the skin, jaundice, microcephaly, and seizures. Laboratory abnormalities include abnormal blood counts (especially thrombocytopenia), hemolytic anemia, elevated transaminases, and elevated serum bilirubin. CT scan of brain reveals periventricular calcifications. Other significant features include progressive sensorineural hearing loss (most com on manifestation) and chorioretinitis.
Congenital rubella syndrome (CRS) can cause multiple severe problems in infants; look for a reference to the mother having had a rash during pregnancy. The most common congenital anomalies include sensorineural deafness (60 to 75%) cataracts (white reflex), cardiac malformations such as patent ductus arteriosus or pulmonary artery stenosis, and neurologic sequelae such as meningoencephalitis, behavior disorders, and mental retardation. Infants born with CRS may manifest with intrauterine growth retardation, microcephaly, hepatosplenomegaly, thrombocytopenia, and characteristic purpura (the “blueberry-muffin” spots).
The majority of live-born neonates with congenital syphilis are asymptomatic at birth. Congenital syphilis can also cause devastating disease in newborns; look for references to rash involving palms and soles, Hutchinson molars, or bone deformities, including saber shin. Clinical manifestations after birth can be divided into early and late. Early manifestations include cutaneous lesions over the palms and soles, hepatosplenomegaly, jaundice, anemia, and occasionally snuffle (profuse watery nasal discharge) and bony abnormalities. Late manifestations include frontal Bossing, short maxilla, high palatal arch, Hutchinson triad (Hutchinson teeth [blunted upper incisors], interstitial keratitis, and eighth-nerve deafness), saddle nose, and perioral Fissures.
Even though GBS infection is the most common cause of neonatal sepsis and it presents with a sepsis picture similar to that described above, it would not present with granulomatosis infanti septicum (which is characteristic of neonatal listeriosis).
Moreover, Gram stain of the maternal cervical smear would reveal gram- positive cocci (streptococci) and not bacilli.
Neonatal herpes simplex infection can be a devastating- infection of the neonate; look for skin, eye, and mouth vesicles and often prominent neurologic involvement; Even though tuberculous nodules in tuberculosis (TB) would give a similar histologic picture of granuloma with central necrosis, nothing else in this question leads toward the diagnosis of maternal TB. Moreover, TB is transmitted neither transplacentally (like CMV, toxoplasmosis, herpes simplex, syphilis, and rubella) nor directly in- utero (like GBS and Listeria) from mother to fetus. Thus, it does not infect neonates.

Explanation:

Explanation:

Explanation:

Bullous impetigo is a localized skin infection characterized by large bullae; it is caused by a group 2 phage type of staphyococcus aureus. Cultures of fluid from an intact blister will reveal the causative agent. Ordinary penicillin is usually effective in streptococcal impetigo but early treatment does not appear to lessen the occurrence of acute glomerulonephritis.

Explanation:

Clinical diagnosis of bacterial sinusitis requires the following: Prolonged nonspecific upper respiratory signs and symptoms (i.e. severe upper respiratory tract signs and symptoms (i.e., fever 30˚C, facial swelling, and facial pain). This individual does not meet these criteria, so antibiotics should not be used at this time. Although some believe that mucopurulent rhinitis (thick, opaque, or discolored nasal discharge) indicates the presence of bacterial sinusitis, this sign should be recognized as part of the natural course of a nonspecific, uncomplicated viral upper respiratory infection (URI). Sinus radiographs can demonstrate thickened mucosa, infundibular occlusion, and occasional air-fluid levels in uncomplicated viral URI.

Explanation:

Erythema infectiosum is characterized by a prodomal illness usually consisting of malaise, pharyngitis, and low-grade fever, followed by the appearance of a “slapped-cheek” rash. The cause of erythema infectiosum has been identified as parvovirus B19.

Explanation:

Whereas many antibiotics temporarily suppress nasopharyngeal colonization by Haemophilus influenzae type b, only rifampin is effective in eradicating the organism. It should therefore be administered to all attendees and staff of a day-care facility in which two or more children have been diagnosed with disease by H. influenzae, regardless of previous, immunization status. The patients should also receive rifampin before returning to the center. Prophylaxis after a single case is controversial.

Explanation:

Clustered circular lesions with accompanying dysesthesia in a dermatome are cahracteric of herpes zoster, which may occur after a stressful event or infection in both children and adults. For herpes zoster to occur there must be a previous primary varicella infection or immunization. Herpes zoster is less likely to be associated “with significant postherapeutic neuralgia in children than in adults.

Explanation:

Explanation:

The positive monospot test indicates atypical lymphocytes that this is infectious mononucleosis as a result of Epstein-Barr infection. Blood smears of EBV mononucleosis reveal a number of atypical lymphocytes.

Explanation:

Perinatal hepatitis B is not associated with mental retardation. Rubella, cytomegalovirus, Toxoplasma gondii, and Herpes simplex are all part of the TORCH syndrome of perinatal infections, all of which include mental retardation as a major manifestation.

Explanation:

Pseudomonas infection is characterized by a foul-smelling discharge. This bacterium has been readily cultured from sneakers, and wounds that occur through sneakers should be considered to be infected by pseudomonas until proven otherwise.

Explanation:

Neisseria meningitidis is not a common cause of neonatal meningitis, while all of the others are.

Explanation:

Yersinia enterocolitica is the pathogen producing this clinical syndrome. Yersinia is transmitted to patients via the oral route most commonly from contaminated pork or milk, and, on occasion, from blood transfusion. It is associated with cooler climates and is a cause of pseudoappendicitis in children. Arthropod vectors are not involved in transmission of Y. enterocolitica. Arthropods such as ticks transmit tularemia, Rocky Mountain spotted fever, and Lyme disease. Insects such as mosquitoes transmit viral encephalitides and malaria. Contaminated ground beef is involved in the transmission of enterohemorrhagic Escherichia coil (EHEC), but is not a common source of infection with Y. enterocolitica. Dog bite is not involved in the transmission of Y. enterocolitica. Dogs may transmit rabies Capnocytophaga or Pasteurella. Endogenous transmission is important in the formation of intestinal abscesses by anaerobic normal flora organisms, but is not believed to be involved with Y. enterocolitica transmission.

Explanation:

Parvoviruses are small single-stranded DNA viruses of which only serotype B19 is pathogenic for humans. This virus causes three distinct syndromes: a childhood febrile rash known as erythema infectiosum (Fifth disease); aplastic crisis in individuals with chronic hemolytic diseases (sickle-cell anemia thalassemia, etc.); and congenital infections can present as stillbirth hydrops fetalis (analogous to severe Rh incompatibility), or severe anemia. Coxsackie viruses usually cause cold like illness but can cause herpangina, myocarditis, and meningitis. Echoviruses can infect a variety of organ systems (gastrointestinal, CNS, eyes, heart, respiratory, skin), but are not a cause of aplastic crises. Hepadnavirus is the causative agent of hepatitis B. Herpes viruses cause a variety of acute to chronic infections including herpes simplex types I and II, chickenpox, chronic herpes zoster, CMV infection, and Epstein-Barr virus infections.

Explanation:

Explanation:

This patient has adrenoleukodystrophy, an X- linked disease that results from mutations that prevent transport of very long-chain fatty acids (VLCFA) into peroxisomes, thereby preventing beta-oxidation and breakdown of VLCFA. Accumulation of abnormal VLCFA in effected organs (neurons and the adrenal cortex) is thought to be the underlying cause of the disorder. Patients thus present with:

Neurologic deficits: begins with weakness and spasticity; proceeds to dementia, blindness, and quadriparesis.
Primary adrenal insufficiency: hyponatremia, postural hypotension, hyperkalemia, and lack of response to the cosyntropin stimulation test Glycerol trierucate has not been shown to slow the progression of disease once onset has been documented. Overall it is not effective, although it may delay the onset of symptoms. Possible new therapies include lovastatin and 4-butyric acid analogues, which induce a protein capable of partially taking over the role of the defective peroxisomal membrane protein. Magnetic resonance of the brain shows lesions throughout the white matter, so it is unusual to have normal findings on MRI. Neurologic Findings may precede the diagnosis of adrenal insufficiency; however, in the majority of cases, adrenal disease is detected before neurologic findings. The responsible gene is a peroxisomal membrane protein, not mitochondrial membrane protein.

Explanation:

This patient has a syphilitic chancre and should be treated with benzathine penicillin G, 2.4 million units intramuscularly in a single dose. Because sexual partners might be infected even if they are seronegative, presumptive treatment should be given to those who were exposed within 90 days.
Benzathine penicillin G, 7.2 million units total administered as three doses is incorrect because this is the appropriate therapy for late latent syphilis or latent syphilis of unknown duration. Latent syphilis is characterized by seroreactivity without evidence of disease. Late latent syphilis is typically defined as latent syphilis that has been present for more than 1 year.
The patient in this case has a chancre, which represents a primary infection and not a latent infection. Because of his history of sexually transmitted disease (STD) he should be encouraged to have an HIV test Because this patient´s serology shows that he has a distant, resolved hepatitis B infection (meaning that he no longer has the disease), it is not necessary for his current sexual partners to receive post exposure prophylaxis against hepatitis B. In warts, treatment may reduce the infectivity but does not typically eradicate the infection

Explanation:

The diagnosis is staphylococcal scalded skin syndrome (SSSS) and it occurs in children under 5 years of age. The beginning of the illness usually consists of constitutional symptoms and skin tenderness, followed by a diffuse scarlatiniform erythema. This is often brighter in the flexural areas and around orifices, especially the mouth. There may also be flaccid blisters and erosions. Under gentle tangential pressure on any area of the skin, there may be separation of the epidermis. This is known as Nikolsky sign and may be seen in toxic epidermal necrolysis (but only at sites of erythema). As large areas of epidermis denude, most skin is exposed, which may become secondarily infected and lead to significant fluid and electrolyte losses. This phase starts from 2 to 5 days after the initial erythema and the disease resolves within 2 weeks without scarring. There is no involvement of the intraoral mucosa; however, the lips may be involved and there may be bilateral purulent conjunctivitis. The disease is caused mostly by phage group 2 staphylococci with hematogenous spread. The bacteria produce epidermolytic or exfoliative toxins A or B. Intact bullae are sterile, which will differentiate from Bullous imetigo. Skin biopsy will show the subcorneal, granular split of the epidermis. With diffuse involvement, an intravenous penicillinase-resistant penicillin such as nafcillin or oxacillin should be administered along with fluids. The skin is also moistened and cleaned with isotonic saline or a Burrow solution. An emollient adds lubrication and aids in comfort. Topical antibiotics are not needed.
Oral amoxicillin would not be effective against staphylococci, and in this case an intravenous antibiotic would be warranted.
Intravenous ampicillin is not penicillinase resistant. Ceftriaxone is a third-generation cephalosporin and as such would not be expected to have much gram-positive coverage.
Ciprofloxacin is contraindicated in children due to potential of cartilage damage. Preparations may be used topically while the macrolides such as erythromycin may be effective against a staphylococcal infection, this case warrants intravenous antibiotics.
Erythema toxicum is a self-limited disease and does not really require treatment.

Explanation:

This patient presents with failure to thrive, developmental delay, fever, oral thrush, an ear infection, and generalized lymphadenopathy. She has a positive risk factor for human immunodeficiency virus (HIV) infection in that her mother has a substance abuse problem. Together, these findings most likely indicate this patient has acquired immune deficiency syndrome (AIDS). AIDS may be caused by the HIV type 1 or type 2. In children, infection with HIV type 2 is rarely found. Most HIV-infected children are born in developing countries and the majority of cases are acquired via vertical transmission from mother to child. Breastfeeding is also a significant route of transmission. Cesarean section combined with prenatal, intrapartum, and neonatal zidovudine therapy significantly reduces transmission of the virus. Sexual contact is a major route of transmission in adolescents. Three patterns of disease have been described in children:
1) HIV-infected newborns with rapid onset of symptoms and acquired immune deficiency syndrome in the first few months of life
2) Prenatally infected newborns with slower progression of disease
3) Long-term survivor with minimal or no progression of disease and normal CD4 counts.
Clinical status and degree of immunologic impairment are used to classify HIV in children. In the majority of infants, the physical examination at birth is normal. However, over a period of time the infant may develop failure to thrive. Problems such as lymphoid interstitial pneumonia, chronic otitis media, persistent diarrhea, hepatosplenomegaly, recurrent bacterial sepsis, and candidiasis may be seen. Older children have similar findings as adults. Detection of antibodies is performed by enzyme-linked immunosorbent assay (ELISA) and Western blot analysis. Passively acquired maternal antibodies last up to 15 months. All infants born to HIV-positive mothers have positive antibody tests at birth because of passive transfer of maternal antibodies. HIV DNA polymerase chain reaction is the preferred virologic assay for infants in developing countries. HIV culture is not recommended for infants less than 1 month of age because of potential for false positive results. HIV disease can be excluded in children over 18 months of age who have at least two HIV antibody tests that are negative, absence of hypogammaglobulinemia, and no clinical evidence of HIV disease. Treatment with antiretroviral therapy in children infected with HIV depends on the viral load, CD4 count and percentage, and clinical condition. Decisions regarding therapy should be made in consultation with an expert in pediatric HIV disease. Opportunistic infection should be treated as the child develops and nutritional support should be given.
Disseminated herpes simplex virus infection is most commonly seen in children between 6 months and 3 years of age. It starts with a severe herpetic gingivostomatitis followed by dissemination to the liver and other internal organs. Massive viremia may ensue with gastroenteritis, encephalitis, and hepatic and adrenal dysfunction.
Death frequently occurs during the phase of massive viremia.
Umbilicated vesicles that evolve into necrotic ulcers may be seen on the skin and mucosal surfaces. Disseminated herpes simplex virus infection may occur in premature newborns, malnourished infants, or patients treated with immunosuppressive drugs, as well as in Wiskott-Aldrich syndrome. Treatment is with intravenous acyclovir.
Infectious mononucleosis is characterized by fever, adenopathy, splenomegaly, lymphocytosis with atypical lymphocytes, and evidence of acute infection by Epstein-Barr virus. After an incubation period of 3 to 7 weeks, bilateral enlargement of the cervical lymph nodes and, at times, of the axillary and inguinal lymph nodes develops with accompanying fever as high as 40 °C (104 °F), malaise, and headache. Pharyngitis is the most frequent sign, with hyperplasia of the pharyngeal lymphoid tissue. Diagnosis is confirmed with the monospot test. Treatment is supportive with rest and avoidance of contact sports until the splenomegaly has resolved.
Streptococcal pharyngitis presents with sudden-onset fever and sore throat. Physical examination reveals very enlarged, erythematous, edematous tonsils covered with purulent exudate. The submandibular lymph nodes may be enlarged and tender. Diagnosis is confirmed with a pharyngeal bacterial culture. The treatment of choice is penicillin.
Systemic candidiasis is a severe, destructive, disseminated disease that occurs in the setting of compromised host defenses.
Hemorrhagic pustules, necrotic ulcers, and deep abscesses are seen on the skin and mucosal surfaces. Other clinical findings depend on organ involvement and may include gastrointestinal bleeding, fever of unknown origin, pulmonary infiltration, endocarditis, renal failure, meningitis, osteomyelitis, endophthalmitis, peritonitis, or a disseminated maculopapular exanthem. Diagnosis is made by demonstrating microorganisms or a positive culture from tissue or fluids that are normally sterile. Mortality is approximately 40%. The standard treatment is amphotericin B, although multiple other systemic antifungal agents are available on the market today.

Explanation:

This baby has infant botulism (floppy baby syndrome), which is due to germination of Clostridium botulinum spores in the baby´s gastrointestinal tract. This disorder is most common in children under the age of 6 months. Older children and adults do not appear to be vulnerable to this form of botulism, but are susceptible to botulism caused by ingestion of preformed toxin. Floppy baby syndrome is acquired following the ingestion of spores of the organism. Dipicolinic acid and calcium dipicolinate are unique to bacterial spores. The former is thought to be responsible for the heat resistance of the spore, while the later helps to stabilize the DNA. A gram positive vegetative bacillus describes Clostridium botulinum, but it is not ingestion of the vegetative bacteria that causes this condition. A neurotoxin encoded on a nonconjugative plasmid describes tetanospasmin, which is produced by Clostridium tetani. This toxin causes a rigid paralysis due to the inhibition of glycine and GABA at inhibitory synapses.
A neurotoxin encoded in a phage genome would describe the botulinum toxin erythrogenic exotoxins of Streptococcus pyogenes and the diphtheria toxin. It is not ingestion of the preformed toxin that causes floppy baby syndrome; it is ingestion of spores. A 150,000 molecular weight progenitor neurotoxin is a description of both the botulinum toxin and the tetanospasmin, but it is not the toxin that is ingested to cause floppy baby syndrome, but the spore of the bacterium.

Explanation:

The rash described is that of scarlet fever, which can be a complication of streptococcal sore throat (as in this question) or streptococcal wound infection. In past centuries, scarlet fever was a major childhood disease that often caused death, but it has become much less common (possibly, as a result of early antibiotic therapy) and is now only a rare cause of death. Strains of streptococci that cause scarlet fever are beta hemolytic group A streptococci that have been infected by a phage. The precise role of the phage is still unclear but may involve up regulation of toxin producing genes because some of the streptococcal strains that do not produce scarlet fever still carry genes for toxin production. Lipopolysaccharide is found in gram-negative organisms. Spore formation is a feature of Bacillus and Clostridium. Mycoplasma are organisms that lack cell walls. Lecithinase is an enzyme produced by Clostridium.

Explanation:

Explanation:

Explanation:

This neonate is most likely suffering from sepsis with or without meningitis, as indicated by respiratory distress (grunting, retractions), bradycardia, temperature instability, poor feeding, lethargy/irritability, vomiting, and diarrhea. Note that the findings of a full (normal), rather than a bulging, fontanelle and of normal neck flexion do not rule out meningitis as the diagnosis because at the time of initial presentation of neonatal meningitis, only 25% of patients present with a bulging fontanelle and only 15% with nuchal rigidity. The clinical presentation of neonatal meningitis is often indistinguishable from that of neonatal sepsis without meningitis, so the diagnosis of sepsis with or without meningitis is confirmed by blood and CSF findings. One of the most common causes of meningitis among neonates and infants up to the age of 3 months old is Listeria monocytogenes. Other agents responsible for meningitis in this age group include Escherichia coli and Group B Streptococcus. Neonates and the elderly have decreased T-cell immune function; therefore, Listeria is more common in the very young and the very old.
Borrelia burgdorferi is not as common as Listeria among neonates and infants. B. burgdorferi is the etiologic agent behind Lyme disease, a zoonotic disease transmitted by ticks. The question will usually give a clue, such as a tick-bite or an annular red rash (the erythema migrans rash that occurs at the site of the tick bite), or a patient from Connecticut, Massachusetts, or New York.
Cryptococcus neoformans is a fungus that occurs primarily in patients who are immunocompromised, such as those who are HIV-positive. . Cryptococcus is usually associated with those HIV-positive patients who have profound decreases in their T-cell counts to levels less than 100 cells.
Mycobacterium tuberculosis is incorrect; there is nothing in the question stem that points toward this etiologic agent (such as a history of TB, cough, weight loss, or night sweats). It is not as common as Listeria among neonates and infants.
Neisseria meningitidis is the most common cause of meningitis among adolescents and young adults. It is spread by respiratory droplets, and results in the characteristic petechial rash. It is not the most common cause of meningitis among neonates and infants.
Streptococcus pneumoniae is the most common cause of meningitis overall; however, it is not the most common cause of meningitis among neonates and infants. Also note that the respiratory distress in the patient is due to neonatal sepsis, and not necessarily to pneumonia.
Treponema pallidum is the causative agent behind syphilis. It is not the most common cause of meningitis among neonates or infants. Congenital syphilis is divided into early and late stages.
Early-stage manifestations appear before 2 years of age and include fever, anemia, failure to thrive, a maculopapular rash, snuffles, hepatosplenomegaly, periostitis of the long bones, and thrombocytopenia. Late-stage manifestations are skeletal and include saber shin, Hutchinson teeth, saddle nose, and knee synovitis.
Rotavirus is the most common cause of gastroenteritis in children. It presents with diarrhea, vomiting, and fever. It rarely affects infants less than 6 months of age with severe symptoms. It can never cause sepsis. The present patient is clearly septic.

Explanation:

The patient described in the question is infected with Entamoeba histolytic the symptoms of which can range from completely asymptomatic (cyst shedding) to intestinal amebiasis to extraintestinal disease. Typically a 2-week incubation period is present after which diarrhea can present, sometimes progressing to colitis in children younger than age 5 years. A chronic form of amebic colitis can develop, mimicking inflammatory bowel disease. Disseminated amebiasis can occur and is a very serious complication of the infection, resulting in liver abscess formation. That is the reason an abdominal ultrasound must be done to evaluate for a hepatic abscess.
Treatment is metronidazole, followed by paromomycin, or iodoquinol.
A barium enema is contraindicated in a patient who has colitis because of the increased risk for developing toxic megacolon or perforation.
Colonic biopsy may show the amebic organisms, but it is not the next most appropriate step in management.
Gallium scan may help in finding the liver abscess, but it is not more cost-effective than an ultrasound.
Liver function tests would be normal, because the abscess formation does not destroy the actual liver cells.

Explanation:

The rare disease illustrated is subacute sclerosing panencephalitis(SSPE),which typically presents as in the question stem. SSPE appears to be due to a combination of persistent, possibly abnormal measles virus and to autoimmune damage caused by antibodies directed against the virus. Many patients developing SSPE have had measles at 2 years of age or younger; there is typically a six-year interval between measles infection and symptom development. A small proportion of cases have followed vaccination with live measles virus. Unfortunately, no effective therapy has been developed, although some experimental work with drugs such as isoprinosine shows some promise. Post infectious encephalomyelitis, rather than SSPE, can follow mumps or varicella. Latent infection with the varicella virus causes shingles (herpes zoster). Papilloma viruses are associated with warts. They do not usually infect the brain. Poliovirus causes gastrointestinal disturbances viremia, and paralysis.

Explanation:

Explanation:

This patient has acquired cat scratch disease, which is caused by the gram negative rod, Bartonella henselae. Bartonella henselae and B. quintana are also responsible for the production of bacillary angiomatosis, which is a vascular proliferative disease involving skin, bone, and subcutaneous tissues in immunocompromised patients. Oroya fever is an acute febrile illness with severe anemia caused by Bartonella bacilliformis. Rat bite fever is caused by Streptobacillus moniliformis, which is a gram-negative bacillus unrelated to the genus bartonella. Trench fever is a febrile illness caused by Bartonella quintana which is transmitted by the human body louse. Verruga is the chronic cutaneous form of Oroya fever, which is caused by Bartonella bacilliformis.

Explanation:

Explanation:

This patient is suffering from a classic case of molluscum contagiosum (MC). MC is caused by the molluscum p. contagiosum virus, which is a member of the Poxviridae family of viruses; Poxviridae are large, boxcar-shaped, enveloped dsDNA viruses.
MC is a very common viral infection, with up to one-quarter of the population showing serologic evidence of past infection. This condition can affect children or adults and can be contracted following casual or sexual contact. The overwhelming majority of cases in children are not due to sexual abuse. The typical clinical presentation is with red-to- pink, glossy papules with indented or umbilicated centers. The eruption is often slightly itchy, and scratching causes spread of the infection through autoinoculation (Koebnerization), resulting in linear aggregations of papules. A mild eczematous eruption known as molluscum dermatitis can frequently form surrounding the papules.
The cowpox virus is the cause of milker´s nodules. It is also known as the vaccinia virus and was used as the first form of vaccination against smallpox. Historically, the fingers, hands, and forearms of people who handled infected cow udders developed solitary or multiple large vesicular lesions.
The Orf virus is a poxvirus that causes a disease known as Orf. Orf is a zoonosis contracted after contact with infected animals, typically livestock. The associated lesions typically are solitary or few and tend to affect the fingers.
The varicella zoster virus which causes chickenpox and shingles is a herpesvirus (HHV3). The eruption in chickenpox manifests as recurrent crops of lesions that resemble “dewdrops on a rose petal. The variola Vera virus which causes smallpox is a member of the Poxviridae family of viruses. Smallpox is a disease that is considered eradicated worldwide but is still of significance due to its potential for use in biologic warfare. The eruption is characterized by a single, diffuse crop of macules evolving to vesicles and ultimately pustules.

Explanation:

This child has developed neonatal sepsis. Sepsis is a systemic response to infection. In newborns it can be classified as early-onset, occurring in the first week of life; and late-onset occurring between age 8 and 28 days. Risk factors for neonatal sepsis include maternal infection during pregnancy (urinary tract infection, chorioamnionitis), prematurity, and prolonged rupture of membranes. Common organisms causing, sepsis in the newborn are group B streptococci, Escherichia coli, and Listeria. Viral causes can be herpes simplex virus and enteroviruses. Signs and symptoms of neonatal sepsis are nonspecific, such as grunting, tachypnea, cyanosis, poor feeding, irritability, apnea, bradycardia, jitters, tremors, and seizures. Newborns do not always develop fever, and hypothermia may be a presenting sign. A bulging fontanelle may be palpated on physical exam, but there is rarely nuchal rigidity. Laboratory studies should include a complete blood count lumbar-puncture, and blood and urine cultures, as well as cultures of any visible lesions or drainage. A chest radiograph should be done to exclude pneumonia. Treatment consists of antibiotics that should be started empirically in expectation of culture and sensitivity studies.
Congenital rubella occurs in 80% of babies if the mother is infected during the first trimester. The most common manifestation is intrauterine growth retardation, followed by congenital cataracts, mental retardation, heart defects (patent ductus arteriosus, pulmonary stenosis), hepatosplenomegaly, deafness, and blueberry-muffin” lesions (foci of extramedullary hematopoiesis). Diagnosis is made by culture or IgM titers. Immunization of the mother prevents disease.
Congenital syphilis appears before 2 years of age and includes fever, anemia, failure to thrive, maculopapular, rashes snuffles, hepatosplenomegaly, periostitis of the long bones, and thrombocytopenia. It is a consequence of transmission from the mother within the first 4 months of pregnancy.
Congenital toxoplasmosis is less; common but more serious if the maternal infection happened in the first trimester of pregnancy and more common but less severe if the maternal infection occurs in the third trimester. It manifests with intracranial calcifications, intrauterine growth retardation, microcephaly, seizures, blindness, and hepatosplenomegaly. Diagnosis is made from cultures and determination of IgM titers. Treatment for the pregnant woman in the first trimester is spiramycin, and pyrimethamine and sulfonamide thereafter. The newborn is treated with pyrimethamine, sulfonamide, and leucovorin. If the neonate has chorioretinitis, steroids are administered with the goal of preventing blindness. Infection with toxoplasmosis is acquired through eating undercooked or raw infected meat or from handling infected cat feces. Neonatal herpes simplex virus infection is usually acquired during passage through in infected birth canal. Primary disease in the mother has a much higher transmission rate to the neonate than recurrent disease.
Delivery by cesarean section should be performed if there are active genital lesions in the mother. Infection may follow three general patterns: local (skin, eye, and mouth), appearing at 5 to 14 days; disseminated (pneumonia, shock, hepatitis), at 5 to 7 days; and central nervous system (lethargy, seizures), at 3 to 4 weeks.
Mortality is high with disseminated disease. Diagnosis can be made by clinical pattern, culture, polymerase chain reaction of the cerebrospinal Fluid, and demonstration of antibodies. Treatment of choice is acyclovir.

Explanation:

Infant botulism results from the production of toxin after colonization of the gastrointestinal tract by Clostridium botulinum in young children aged 1-9 months. The most common source of the organism is the soil or, less frequently, honey. Nearly all cases are due to types A or B. The incubation period is usually between 18 and 36 hours. Short incubation periods are associated with more severe disease. The disease spectrum varies considerably but the most commonly recognized form is the “floppy baby syndrome: Initial symptoms are lethargy, diminished suck, constipation, weakness, feeble cry, and diminished spontaneous activity with loss of head control.

These symptoms are followed by extensive flaccid paralysis. The case fatality rate is only 1 %. The bulbar musculature is usually affected first. In older children, it results in diplopia, dysarthria, and dysphagia. Involvement of the cholinergic autonomic nervous system may result in decreased salivation, with dry mouth and sore throat, ileus, or urinary retention. Neurologic evaluation often shows bilateral paresis of the 6th cranial nerves, ptosis, dilated pupils with sluggish reaction, decreased gag reflex, or medial rectus paresis. These symptoms are followed by descending involvement of motor neurons to peripheral muscles, including the muscles of respiration. Patients are usually febrile with clear mentation. The most common cause of death is respiratory failure. The spectrum of disease is quite variable; some patients have mild disease, whereas others have severe paralysis requiring mechanical ventilation. Respiratory failure is the major risk, and patients must be monitored carefully with liberal use of ventilatory support. Toxins can be removed from the gastrointestinal tract with gastric lavage, cathartics, and enemas early in the course of disease. The trivalent antitoxin or type-specific antitoxin for types A, B, and E is usually given only to adults. Infants with botulism should not receive either antibiotic directed against C.

Botulinum or antitoxin, because most do extremely well with supportive care alone and it has been suggested that antibiotics may cause toxin release. Honey has been implicated as a vehicle for spores and should not be fed to infants younger than 1 year.

Congenital hypothyroidism, or cretinism, manifests as impaired development of the skeletal system and CNS. It is associated with severe mental retardation, short stature, coarse facial features, a protruding tongue, and umbilical hernia.

Guillain-Barre syndrome presents with weakness that develops symmetrically over several days. The weakness typically occurs first in the legs and ascends with time to involve the muscles of the trunk, intercostals, upper extremity, and neck. Muscles innervated by cranial nerves are also involved. Respiratory paralysis can lead to death within hours to days.

Myasthenia gravis is a disorder of the neuromuscular junction resulting in a pure motor syndrome characterized by weakness and fatigue, particularly of the extraocular, pharyngeal, facial, cervical, proximal limb, and respiratory musculature. Fifteen percent of infants born to myasthenic mothers have neonatal myasthenia gravis because of the transplacental passage of acetylcholine receptor antibodies. The condition completely resolves in weeks to months.

Vaccine-associated poliomyelitis is exceedingly rare; only eight or nine cases are reported yearly. Most symptomatic cases have nonspecific manifestations of infection illness is biphasic, and paralysis occurs in the second phase. Paralytic disease occurs with rapid onset, involving the cranial nerves, arms, and legs.

Explanation:

Neonatal conjunctivitis is purulent ocular drainage due to a chemical irritant or a pathogenic organism. Topical prevention is routine. Chlamydial ophthalmia usually occurs 5 to 14 days after birth. It may range from mild conjunctivitis with minimal mucopurulent discharge to severe eyelid edema with copious drainage and pseudomembrane formation. Follicles are not present in the conjunctiva, as they are in older children and adults.
In chlamydial ophthalmia, systemic-therapy is the treatment of choice ´because at least 1/2 of affected neonates also have nasopharyngeal infection and some develop chlamydial pneumonia. Erythromycin 12.5 mg/kg po q 6 h for 2 weeks is recommended. Efficacy of this therapy is only 80%, so a 2nd treatment course may be needed.

Explanation:

The most common infection transmitted person to-person in wrestlers is herpes gladiatorum caused by the herpes simplex virus. Molluscum contagiosum causes keratinized plugs. Human papillomavirus causes warts. Tinea corporis is ringworm, which is manifested by round tm oval raised areas with central clearing. Mat burn is an abrasion.

Explanation:

The most common cause of infant botulism is ingestion of Clostridium botulium spores in honey.

Explanation:

This boy has developed mumps. The most common complication in prepubertal children is meningoencephalomyelitis due to spread of infection in the CNS. Mumps is a viral infection with a paramyxovirus that causes painful enlargement of the salivary glands, predominantly the parotid glands. Transmission of the mumps virus occurs via airborne droplets, direct contact and fomites contaminated with saliva. It is more common in the winter and spring. Outbreaks are related to lack of immunization. The treatment of mumps is supportive. This is a viral infection and not related to streptococcal meningitis.
Dacryoadenitis is a rare complication of mumps in which the lacrimal gland and duct are inflamed as a consequence of the viral infection.
Infertility is not a common complication of mumps, even with bilateral orchitis. Mumps oophoritis may develop in postpubertal females but it does not affect fertility.
Orchitis is an uncommon complication in prepubertal children, even though it is the most common complication in adult males. It may be unilateral or bilateral and is treated with support and bed rest. In 30% of cases it may be bilateral. Even in those cases, infertility is rare.

Explanation:

One of the most common causes of meningitis among neonates and infants up to the age of 3 months is Group B Streptococcus (GBS), otherwise known as Streptococcus agalactiae. Other agents responsible for meningitis in this age group include Escherichia coli and Listeria monocytogenes. CSF findings indicate bacterial pattern.
Borrelia burgdorferi is not as common as GBS among neonates and infants. S. burgdorferi is the etiologic agent behind Lyme disease, a zoonotic disease transmitted by ticks. The question will usually give a clue, such as a tick bite or an annular red rash (the erythema migrans rash that occurs at the site of the tick bite).
Cryptococcus neoformans is a fungus that occurs primarily in patients who are immunocompromised, such as those who are HIV-positive. Although it is common among this patient population, it is not the most common agent to cause meningitis among this population. Cryptococcus is usually associated with those HIV-positive patients who have profound decreases in their T-cell counts to levels less than 100 cells.
Neisseria meningitidis is the most common cause of, meningitis among adolescents and young adults. It is spread by respiratory droplets and results in the characteristic petechial rash. It is less common among neonates and infants before 3 months of age.
Streptococcus pneumoniae is the most common cause of meningitis overall, but it is not the most common cause of meningitis among neonates and infants.
Cytomegalovirus causes meningitis in immunocompromised.

Explanation:

The child is exhibiting signs of meningitis, as demonstrate by his lethargy and fever and confirmed by the elevated protein and decreased glucose in the CSF analysis. The MRI finding of abscesses is what determines the etiologic microorganism to be Citrobacter koseri, which is notorious for abscess formation in 80% of patients. This microorganism is a gram-negative enteric rod, resistant to ampicillin. The mode of transmission is most commonly vertical, from mother to infant during delivery. Treatment is usually a third- or fourth-generation cephalosporin and aminoglycosides for 4 to 6 weeks. The abscess area is frequently drained, with follow-up imaging to determine improvement.
Although Escherichia coli, Klebsiella pneumoniae, Listeria monocytogenes, and Streptococcus agalactiae (group B Streptococcus) can cause a brain abscess, Citrobacter is the most common bacteria causing the indolent course of meningitis described for a neonate with a brain abscess formation.

Explanation:

This patient most likely has herpetic whitlow, a herpes infection at the terminal phalanx caused by herpes simplex virus 1 (HSV-1) and herpes simplex virus 2 (HSV-2). This painful infection of the hand most often involves the index finger or the thumb. In children, infections involving the fingers most often are caused by autoinoculation from primary oral HSV-1 lesions that are spread by finger or thumb sucking. The oral lesions, however, are not always present at the same time as the hand lesions because of the incubation period of the infection. The natural history of herpetic whitlow is to improve on its own in Iwo to two to weeks but many recommend treatment with oral acyclovir (400 mg TID) for ten days.
Although the efficacy of treatment has been unproven it is better to be on the safe side.
Incision and drainage is contraindicated in herpetic whitlow. Incision of the lesions results in delayed resolution that may lead to bacterial superinfection or systemic spread. Major complications may also occur, like herpes encephalitis. Hence, extreme caution should be taken.
Oral amoxicillin and topical bacitracin are not indicated in uncomplicated herpetic whitlow. Both could be indicated in cases of bacterial superinfection.
Topical ketoconazole is not used in herpetic whitlow. They are used for systemic and cutaneous fungal infections, respectively.
Cutaneous fungal infections usually are not associated with vesicular lesions. They are associated more classically with erythematous scaling eruptions.

Explanation:

Unlike meningitis occurring in normal children, ventriculoperitoneal shunt infections are most commonly caused by coagulase-negative Staphylococcus, such as Staphylococcus epidermidis. S. epidermidis causes 40%to 60% of all CSF infections in persons with ventriculoperitoneal shunts. Coagulase-negative Staphylococcus presents a significant threat to people who have indwelling devices or catheters. Most S. epidermidis isolates are resistant to multiple antibiotics, including nafcillin and oxacillin.
Vancomycin is the drug of choice to S. epidermidis infection. Removal of the indwelling medical device and parenteral anticiotic treatment are often necessary.
Kernig´s sign is positive if when the thigh is flexed at a right angle, complete extension of the leg is not possible, or causes exquisite pain. A positive Brudzinski´s sign is when bending of the neck causes flexion of the hips. Both signs are used to test nuchal-rigidity in evaluating patients for meningitis.
Haemophilus influenzae. Neisseria meningitidis, and Streptococcus pneumoniae are the most common pathogens of meningitis in normal hosts.
Pseudomonas aeruginosa is a rare cause of meningitis in children, with or without ventriculoperitoneal shunt.
Streptococcus Agalactiae, a group B streptococcus affects neonates.

Explanation:

This patient most likely has varicella (chickenpox), a primary infection with the varicella zoster virus vesicles, pustules, and crusts in various stages of evolution are the typical findings. Symptomatic treatment with oral rehydration, antipyretics, and topical antipruritic agents can be used. Aspirin is contraindicated with varicella because of the association with Reye syndrome. Varicella usually presents with cutaneous infection in immunocompetent hosts. However, in immunocompromised patients, such as this girl with acute lymphocytic leukemia (ALL), varicella can cause serious and life-threatening complications, such as varicella pneumonia varicella pneumonia has a very poor prognosis in patients with ALL, reaching a mortality of roughly 25%. The clinical course usually deteriorates rapidly and many patients die within 3 days of the diagnosis. Pneumonia is exceedingly rare in normal children, but it can happen in older adults.
IV acyclovir therapy is indicated in immunocompromised patients with varicella infection) Therapy should be initiated early in the disease course to maximize efficacy of the treatment varicella zoster immune globulin (VZIG) may modify the disease course if it is given shortly after the exposure. It is not useful, however, once the disease is established, as in this clinical vignette. Children with varicella also should not be given salicylates because of a theoretically increased risk of subsequent Reye syndrome. Patients should be both contact- and airborne-isolated during the entire course of the illness.
Other, less common, complications include encephalitis, hepatitis, glomerulonephritis, arthritis, and thrombocytopenia.
Cellulitis and endocarditis are not typical complications of varicella infection.

Explanation:

This young man has a nevus sebaceous (of Jadassohn), a hamartoma that clinically presents as a sharply circumscribed, verrucous plaque varying from a few millimeters to several centimeters in diameter. This solitary lesion is always present at birth, most often near the vertex of the scalp, but also may be found on the face or neck, where it is usually linear in shape. It enlarges as the child grows and undergoes change at the onset of puberty when it starts to acquire a verrucous surface and increases in thickness with these changes, an increased risk of benign or malignant tumors developing within the nevus begins. Because malignancy may develop, the treatment of choice is excision at an early age.
Alopecia areata presents as rapid and complete loss of hair in one or, more often, several round or oval patches, usually in the scalp, beard area, eyebrows, or eyelashes. The patches are commonly between 1 and 5 cm in diameter and a few resting hairs may be found within them. There are no epidermal changes presents and the scalp skin appears completely normal except for the absence of hair. The lesions usually persist for several months before new hair growth occurs and, initially, fine, depigmented hairs will grow, to be subsequently replaced by normal hair.
Aplasia cutis congenita is a rare anomaly that presents as a congenital defect of the skin with a predilection for the midline of the vertex of the scalp. At birth a round or oval absence of skin and subcutaneous tissue is seen that subsequently heals from the periphery, and leaving a permanent atrophic and alopecic patch that persists unchanged thereafter. Very large or severe defects may require surgical intervention. Imaging studies of the head are indicated to rule out underlying defects of the cranium or neural tissue.
Inflammatory linear verrucous epidermal nevus is usually present at birth or appears in the first few years of life, and is mainly found on the extremities. Clinically, a linear, erythematous, verrucous, scaly or keratotic plaque that is intensely pruritic and resistant to topical or intralesional treatments is characteristic.
Sebaceous hyperplasia also known as senile sebaceous adenoma, is a common lesion found scattered over the face in the shape of small, cream- or yellow-colored umbilicated papules 2 to 6 mm in size. The age at onset is usually over 40 years. Treatment is for cosmetic purposes and may be done with electrodesiccation or fine electrofulguration. A shave biopsy should be done if there is any doubt about the diagnosis.