Staphylococcal Infections

Background

Staphylococcal infections are usually acquired by the animal Staphylococcus aureus. However, the accident of infections due to Staphylococcus epidermidis and added coagulase-negative staphylococci has been steadily accretion in contempo years. This commodity focuses on S aureus but additionally discusses infections acquired by coagulase-negative staphylococci back important differences exist.

Pathophysiology

S aureus is a gram-positive coccus that is both catalase- and coagulase-positive. Colonies are aureate and acerb hemolytic on claret agar. They aftermath a ambit of toxins, including alpha-toxin, beta-toxin, gamma-toxin, delta-toxin, exfoliatin, enterotoxins, Panton-Valentine leukocidin (PVL), and baneful shock affection toxin–1 (TSST-1). The enterotoxins and TSST-1 are associated with baneful shock syndrome. PVL is associated with baleful skin and lung infections and has been apparent to be a above acerbity agency for pneumonia and osteomyelitis. Coagulase-negative staphylococci, decidedly S epidermidis, aftermath an exopolysaccharide (slime) that promotes foreign-body adherence and attrition to phagocytosis.

Nienaber et al accept approved that methicillin-susceptible S aureus isolates causing endocarditis are added acceptable to be from a specific clonal array (CC30) and to acquire specific acerbity genes as compared to MSSA isolates from the aforementioned regions causing bendable tissue infection. Isolates from patients with endocarditis were added acceptable to acquire genes for 3 altered adhesins and 5 altered enterotoxins. The gene for PVL was begin in the boyhood of both groups.

In a abstraction of 42 Staphylococcus lugdunensis isolates, best isolates were able to anatomy at atomic a anemic biofilm, but the bulk of biofilm formed by isolates was amalgamate with poor alternation amid analytic severity of ache and amount of biofilm formation.

Epidemiology

Frequency

United States

Up to 80% of bodies are eventually colonized with S aureus. Best are colonized abandoned intermittently; 20-30% are agilely colonized. Colonization ante in bloom affliction workers, bodies with diabetes, and patients on dialysis are college than in the accepted population. The antecedent adenoids are the absolute armpit of colonization in adults; carrying actuality has been associated with the development of bacteremia. Added abeyant sites of colonization accommodate the throat, axilla, rectum, and perineum.

International

S aureus infection occurs worldwide. Pyomyositis due to S aureus is added accustomed in the tropics.

Mortality/Morbidity

Mortality due to staphylococcal infections varies widely. Untreated S aureus bacteremia carries a bloodshed amount that exceeds 80%. The bloodshed amount of staphylococcal baneful shock affection is 3-5%. Infections due to coagulase-negative staphylococci usually backpack a actual low bloodshed rate. Because these infections are frequently associated with prosthetic devices, the best austere aggravation is the charge to abolish the circuitous prosthesis, although prosthetic valve endocarditis may advance to death.

Thrombocytopenia is associated with added bloodshed amid patients with S aureus bacteremia.

Race

Staphylococcal infections accept no appear ancestral predilection.

Sex

The vaginal carrying amount of staphylococcal breed is about 10% in premenopausal women. The amount is alike college during menses.

Age

Staphylococcal breed arrive abounding neonates on the skin, perineum, umbilical stump, and GI tract. The staphylococcal colonization amount in adults is about 40% at any accustomed time.

The bloodshed amount of S aureus bacteremia in aged bodies is clearly increased.

Staphylococcal Infections Analytic Presentation

History

Common manifestations of staphylococcal infections accommodate the afterward types of infections. The history acquired usually depends on the blazon of infection the animal causes.

Bark infections (Many individuals who present with community-acquired bark infections are initially misdiagnosed with spider bites. These infections are generally due to methicillin-resistant S aureus [MRSA].)

Folliculitis

Furuncles

Impetigo (bullous)

Wound infections

Scalded bark syndrome

Soft-tissue infections (pyomyositis, catchbasin bursitis, catchbasin arthritis)

Baneful shock syndrome

Purpura fulminans

Endocarditis

Osteomyelitis

Pneumonia

Food poisoning

Infections accompanying to prosthetic devices

Frequently associated with coagulase-negative staphylococci

Includes prosthetic joints and affection valves and vascular shunts, grafts, and catheters

Urinary amplitude infection

Physical

Bark and soft-tissue infections

Erythema

Warmth

Draining atrium tracts

Superficial abscesses

Bullous impetigo

Baneful shock syndrome

Fever greater than 38.9°C

Diffuse erythroderma - Deep, red, "sunburned" appearance

Hypotension

Desquamation - Occurs 7-14 canicule afterwards access of illness, usually involves award and soles

Endocarditis

Regurgitant murmur

Petechiae or added cutaneous lesions.

 

Embolic lesions in accommodating with Staphylococcus aurEmbolic lesions in accommodating with Staphylococcus aureus endocarditis

 

Close-up appearance of embolic lesions in accommodating with SClose-up appearance of embolic lesions in accommodating with Staphylococcus aureus endocarditis.

Fever

Causes

Predisposing factors for staphylococcal infections accommodate the following:

Neutropenia or neutrophil dysfunction

Diabetes

Intravenous biologic abuse

Foreign bodies, including intravascular catheters

Trauma

Colonization with S aureus is common. Skin-to-skin and skin-to-fomite acquaintance are accepted routes of acquisition. Isolates can be advance by coughing or sneezing.Evidence has additionally apparent that S aureus can be advance during macho homosexual sex. Pets can additionally serve as domiciliary reservoirs.

Staphylococcal Infections Analysis & Management

Medical Care

Promptly alpha antimicrobial analysis back S aureus infection is accurate or acerb suspected. Appropriate choices depend on bounded susceptibility patterns. Admission of subinhibitory concentrations of antibiotics may advance to added assembly of PVL. The Infectious Diseases Society of America has appear abundant guidelines on the analysis of methicillin-resistant S aureus infections.

Temporary intravascular accessories should be promptly removed if infection is suspected. Long-term intravascular accessories should be removed if infection with S aureus is documented.

Multiple decolonization regimens accept been acclimated in patients with alternate staphylococcal infection. Analysis with contemporary mupirocin, chlorhexidine gluconate washes, and articulate rifampin additional doxycycline for 7 canicule eradicated methicillin-resistant S aureus (MRSA) colonization in ailing patients.

Surgical Care

Abscesses charge be drained. Infections involving a prosthetic collective usually crave abatement of the prosthesis. Added infections involving a prosthetic device, such as a prosthetic affection valve or built-in intravascular device, may or may not crave abatement of the device.

Medication Summary

Historically, isolates aggressive to oxacillin (commonly referred to as methicillin-resistant S aureus [MRSA]) were aggressive to best agents added than vancomycin, but these isolates were bound to nosocomial infections. Added recently, abounding letters accept declared community-acquired MRSA infections that accept been affected to assorted non–beta-lactam antibiotics. As such, patients with austere staphylococcal infections should be initially started on agents alive adjoin MRSA until susceptibility after-effects are available. Abounding coagulase-negative staphylococci are oxacillin-resistant. The continuance of analysis and the use of accessory combinations depend on the blazon of infection encountered. Endocarditis due to S aureus may crave a abiding advance of antibiotics.

Although abounding strains of MRSA that account community-acquired infection are affected to trimethoprim-sulfamethoxazole, analysis with trimethoprim-sulfamethoxazole has been associated with analytic failure, abnormally in the attendance of cogent tissue damage.

Vancomycin-resistant isolates accept been reported; isolates with an added minimum inhibitory absorption (MIC) to vancomycin are acceptable added accepted and accommodate both MRSA and methicillin-susceptible S aureus (MSSA). Consensus guidelines acclaim dosing vancomycin to abstain a canal of beneath than 10 mcg/mL; canal levels of 15-20 mcg/mL are recommended to amusement complicated infections

In a abstraction of 296 afterwards MRSA bacteremia episodes, several factors were predictive of aerial vancomycin MIC, including age earlier than 50 years, above-mentioned vancomycin exposure, history of MRSA bacteremia, history of abiding alarmist disease, and attendance of a nontunneled catheter.

Antibiotics

Class Summary

Empiric antimicrobial analysis charge be absolute and should awning all acceptable bacilli in the ambience of the analytic setting.

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Nafcillin (Nafcil, Unipen, Nallpen)

Preferred analysis for methicillin-susceptible S aureus (MSSA) staphylococci infections. Use parenteral analysis initially in astringent infections. Oxacillin may be commissioned for nafcillin based on hospital formulary. Change to articulate analysis as activity warrants.

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Vancomycin (Vancocin, Vancoled)

Indicated for patients who cannot accept penicillins and cephalosporins or accept infections with aggressive staphylococci. To abate the accident for toxicity, appraisal vancomycin canal levels afterwards third dosage fatigued 0.5 h above-mentioned to abutting dosing. Use CrCl to acclimatize dosage in patients diagnosed with renal impairment.

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Telavancin (Vibativ)

Lipoglycopeptide antibacterial that is a constructed acquired of vancomycin. Inhibits bacterial corpuscle bank amalgam by interfering with polymerization and cross-linking of peptidoglycan. Unlike vancomycin, telavancin additionally depolarizes the bacterial corpuscle film and disrupts its anatomic integrity. Adumbrated for complicated bark and bark anatomy infections acquired by affected gram-positive bacteria, including Staphylococcus aureus (both methicillin-resistant and methicillin-susceptible strains), Streptococcus pyogenes, Streptococcus agalactiae, Streptococcus anginosus group, and Enterococcus faecalis (vancomycin-susceptible isolates only).

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Cefazolin (Ancef, Kefzol)

First-generation semisynthetic cephalosporin that arrests bacterial corpuscle bank synthesis, inhibiting bacterial growth. Primarily alive adjoin bark flora, including S aureus (MSSA). Typically acclimated abandoned for bark and skin-structure coverage. IV and IM dosing regimens are similar.

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Clindamycin (Cleocin)

Lincosamide for analysis of austere bark and bendable tissue staphylococci infections. Additionally able adjoin aerobic and anaerobic streptococci (except enterococcal) (MSSA). Inhibits bacterial growth, possibly by blocking break of peptidyl t-RNA from ribosomes, causing RNA-dependent protein amalgam to arrest.

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Dicloxacillin (Dycill, Dynapen)

Binds to one or added penicillin-binding proteins, which, in turn, inhibits amalgam of bacterial corpuscle walls. For analysis of infections acquired by penicillinase-producing staphylococci affected to methicillin (MSSA). Additionally alive adjoin best nonenterococcal streptococci. May use to admit analysis back staphylococcal infection is suggested.

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Trimethoprim-sulfamethoxazole (Bactrim, Bactrim DS, Septra, Septra DS)

Inhibits bacterial advance by inhibiting amalgam of dihydrofolic acid. Alive adjoin best staphylococci (MSSA), including some strains aggressive to methicillin (MRSA).

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Minocycline (Minocin)

Inhibits protein amalgam and appropriately bacterial advance by bounden to 30S and possibly 50S ribosomal subunits of affected bacteria. Alive adjoin MSSA/MRSA. Beneath alive adjoin coagulase-negative staphylococci. Doxycycline (Vibramycin) may be acclimated in abode of minocycline

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Linezolid (Zyvox)

Prevents accumulation of anatomic 70S admission complex, which is capital for bacterial adaptation process. Bacteriostatic adjoin staphylococci (MSSA/MRSA).

The FDA warns adjoin the circumstantial use of linezolid with serotonergic psychiatric drugs, unless adumbrated for life-threatening or burning conditions. Linezolid may access serotonin CNS levels as a aftereffect of MAO-A inhibition, accretion the accident of serotonin syndrome.

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Quinupristin/dalfopristin (Synercid)

Belongs to the streptogramin accumulation of antibiotics. Mechanism of activity is agnate to macrolides/lincosamides. Inhibits protein amalgam and is usually bacteriostatic. Additionally an advantage for methicillin-resistant S aureus (MRSA) infections.

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Daptomycin (Cubicin)

Indicated to amusement complicated bark and bark anatomy infections acquired by S aureus (including MRSA strains), Streptococcus pyogenes, Streptococcus agalactiae, Streptococcus dysgalactiae, and Enterococcus faecalis. Additionally adumbrated for right-sided endocarditis due to S aureus. First of fresh antibacterial chic alleged circadian lipopeptides. Binds to bacterial membranes and causes accelerated film abeyant depolarization, thereby inhibiting protein, DNA, and RNA amalgam and ultimately causing corpuscle death.

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Tigecycline (Tygacil)

A glycylcycline antibacterial that is structurally agnate to tetracycline antibiotics. Inhibits bacterial protein adaptation by bounden to 30S ribosomal subunit, and blocks access of amino-acyl tRNA molecules in ribosome A site. Adumbrated for complicated bark and bark anatomy infections and complicated intra-abdominal infections. Alive adjoin S aureus (including MRSA), as able-bodied as best streptococci, enterococci (including VRE), and gram-negative bacilli (including anaerobes).

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Pediatric HIV Infection

Background

Over the accomplished 30 years, back the aboriginal cases of what is now accustomed as animal immunodeficiency virus (HIV) infection were articular in 1981, the cardinal of accouchement adulterated with HIV has added abominably in developing countries because the cardinal of HIV-infected women of bearing age has risen. However, abundant advances accept been fabricated in the United States and in added automated nations to ascendancy manual of the virus from mother to infant.

In the United States, accepted prenatal HIV testing has been recommended to obstetricians back 1995. However, this testing was not binding in all states. Afore prenatal testing was common, diagnosing HIV infections in a woman afterwards diagnosing it in her boyish was not unusual, and the analysis of acquired immunodeficiency affection (AIDS) in a ahead advantageous boyish was not rare.

Before 1985, one way in which accouchement were adulterated was the admixture of blood-products. Improved screening tests accept about abandoned such transmission. A accepted way adolescents become adulterated is by agreeable in high-risk behaviors such as caught intercourse, macho homosexual intercourse, and intravenous (IV) biologic abuse.

Surveillance abstracts now actualization that the abandoned accumulation with accretion HIV accident is men who accept sex with men. The admeasurement of this citizenry who are blind of their infection is high, with blindness amid boyish men (18-29 y) extensive 63%.

In pediatric patients, HIV infection progresses as it does in adults, although surveillance abstracts from the Centers for Ache Ascendancy and Blockage (CDC) advance that patients who are age-old 13-24 years back diagnosed with AIDS survive best than beforehand individuals do. Angular transmitted HIV can annual rapidly progressive, chronically progressive, or adultlike ache in which a cogent analytic cessation aeon occurs afore affection appear.

The Apple Bloom Organization (WHO) estimates that about 2.5 actor accouchement were active with HIV infection as of 2009. In 2009 alone, 370,000 accouchement were anew infected. This is a bead of 24% from 5 years earlier.

Not abandoned are the accouchement themselves ravaged by disease, but their primary caregivers accept additionally generally succumbed to acquired allowed absence affection (AIDS). This is best accustomed in sub-Saharan Africa, area an estimated 11.6 actor accouchement had been orphaned by AIDS as of 2007.

Although 2 strains of HIV accept currently been identified, best patients who accept AIDS are absolute for HIV blazon 1 (HIV-1) or are absolute for both HIV-1 and HIV blazon 2 (HIV-2). HIV-2 infection is best frequently empiric in West Africa.

Vertical manual of HIV from mother to boyish is the capital avenue by which adolescence HIV infection is acquired; the accident of perinatal accretion is 25-40% afterwards intervention Perinatal manual of infection by the mother accounts for 80% of pediatric HIV ache cases in the United States. Perinatal manual can action in utero, during the peripartum period, and from breastfeeding.

Other routes of transmission, such as admixture of claret and claret components, are attenuate in the United States but still abide in developing countries. Sexual corruption of accouchement and high-risk behaviors in adolescents additionally accord to adolescence HIV infection.

A array of signs and affection should active the analyst to the achievability of HIV infection in a child. The presentations accommodate alternate bacterial infections, bound fever, bound diarrhea, bound thrush, alternate pneumonia, abiding parotitis, ambiguous lymphadenopathy, adjournment in development with abortion to thrive, and cogent pruritic dermatoses. Mucocutaneous eruptions may be the aboriginal assurance of HIV infection and may alter in presentation, depending on the child's allowed status.

For advice on HIV infection in adults and adolescents, see HIV Disease.

Pathophysiology

HIV can be transmitted vertically, sexually, or via attenuated claret articles or IV biologic abuse. Vertical HIV infection occurs afore birth, during delivery, or afterwards birth. With infection afore bearing (period 1), the fetus can be hematologically adulterated by agency of manual beyond the placenta or beyond the amniotic membranes, abnormally if the membranes are affronted or infected.

Most vertical infections action during commitment (period 2), and abounding factors affect the accident of infection during this aeon (see Deterrence/Prevention). In general, the best and the greater bulk of acquaintance the boyish has with adulterated affectionate claret and cervicovaginal secretions, the greater the accident of vertical transmission. Premature and low-birthweight neonates arise to accept an added accident of infection during commitment because of their bargain bark barrier and immunologic defenses.

Postnatal vertical manual (period 3) occurs with the assimilation of HIV in the breast milk.

HIV virology

HIV is a retrovirus. Structurally, a lipid bilayer envelope surrounds the annular amount of HIV, which contains the RNA abiogenetic advice and the accouterment that promotes viral archetype and affiliation during antecedent cellular infection. From the outside, the virion appears spherical, with a bore of 110 nm.

HIV has a array of structural and nonstructural proteins that actuate the alternation of the virus with the host's allowed arrangement and cellular components. The genome layouts of HIV-1 and HIV blazon 2 (HIV-2) are apparent in the angel below.

Genome blueprint of animal immunodeficiency virus (HIVGenome blueprint of animal immunodeficiency virus (HIV)–1 and HIV-2. 

The HIV virus attaches to the host corpuscle by the affiliation of a apparent glycoprotein to the CD4 molecule; therefore, it primarily infects CD4+ lymphocytes and macrophages.

After HIV enters a host, trimeric gp120 glycoproteins that beetle from its lipoprotein bilayer envelope bind to CD4 cell-surface receptors and CCR5 or CXCR4 chemokine co-receptors. Juxtapositioned co-receptors are bare for viral infection. The V3 arena of the gp120 glycoprotein determines cellular tropism, and tropism is circuitous in syncytial formation. M-tropic (nonsyncytial) strains adopt the CCR5 co-receptor and are the primary causes of infection.

Deficiency of CCR5 chemokine co-receptors is present in as abounding as 10% of Europeans and 20% of Ashkenazi Jews, and it appears to advise some aegis adjoin infection. Afterwards gp120 binds to the receptors, an associated gp41 transmembrane glycoprotein is amid into the corpuscle film and initiates cell-membrane fusion.

Upon entering the cell, the protease agitator produces the about-face transcriptase and ribonuclease (RNAse) H enzymes amenable for synthesizing the single-stranded DNA (ssDNA) molecules and primers all-important to aftermath the commutual DNA strand. Because about-face transcriptase lacks proofreading capacity, ample base-to-base airheadedness results. The aerial alteration rate, accumulated with the aerial changeable rate, after-effects in abundant change and consecutive attrition to treatment.

Once the virus amount enters the corpuscle cytoplasm of the host, viral about-face transcriptase copies viral RNA to the DNA of the host. The viral DNA is again transported into the basis and congenital into the DNA of that cell. If activated, viral announcement can aftereffect in fresh viral RNA and proteins. Fresh viral amount proteins, enzymes, and viral RNA molecules can abet budding, with added corpuscle infection.

Immune response

Acute infection rapidly increases the viral amount and causes a mild-to-moderate viremia. Although viral endless tend to abate rapidly afterwards astute infection in adults, they abatement boring in angular adulterated accouchement and may not ability baseline levels until age 4-5 years. Although breed admission abundant antigen-presenting and effector beef compared with adults, their cytokine production, proliferation, and cytotoxicity are reduced.

Envelope-specific cytotoxic T-lymphocytes are beneath accepted in accouchement who angular admission the ache than in accouchement who admission HIV by agency of claret transfusion. Amid those with angular acquired disease, lymphocytes are atomic accepted in those with rapidly avant-garde disease. Precursors of cytotoxic T-lymphocyte that are specific to HIV blazon 1 (HIV-1) do not advance in cogent cardinal until the boyish is age-old 1 year.

In adults, antibodies to gp120 advance several months afterwards the antecedent viremia occurs. The development of broadly acrid antibodies is associated with slowed ache progression in adults, children, and infants.

The abridgement in cell-mediated amnesty and accessory B-cell dysfunction aftereffect in the immunocompromised accompaniment and in the admeasurement of adept infections and malignancies. An animated akin of activation-induced corpuscle afterlife consistent from apoptosis of T beef occurs in patients who are HIV positive.

The CD95/Fas receptor/ligand arrangement is all-important for the apoptosis of T cells, and abnormalities in this arrangement are affiliated with added T-cell afterlife in patients who are HIV positive. As the allowed cachet deteriorates, an admission in CD95+ T beef is found; conversely, a low CD95+ T-cell calculation is begin in asymptomatic patients who are HIV positive.

Hematopoietic effects

Although HIV infects hematopoietic axis cells, the accent is minor. Hematopoietic disturbances are believed to action as a aftereffect of changes in the microenvironment of the bottom and of deficiencies in bounded and systemic advance factors.

In archetypal conditions, the stroma of the bottom promotes axis corpuscle admeasurement and adverse by bearing granulocyte colony-stimulating agency (G-CSF) and interleukin (IL)-3. HIV-infected stroma produces beneath G-CSF and IL-3 than accustomed and produces boundless bump afterlife agency (TNF)-alpha and IFN-gamma. This cytokine dysregulation halts the assembly of abominably bare hematopoietic corpuscle curve and causes apoptosis of committed antecedent cells.

HIV additionally appears to arrest the assembly of thrombopoietin in the alarmist and erythropoietin in the kidney. In accession n to a low serum erythropoietin level, HIV-induced anemia is additionally a aftereffect of a blunted acknowledgment to erythropoietin.

Thrombocytopenia occurs in 40% of patients with HIV infection during the advance of the disease. It is best accepted in bodies with avant-garde disease, those who use IV drugs, African Americans, and those with a history of anemia or lymphoma. The attendance of thrombocytopenia suggests a beneath adaptation time.

Immune thrombocytopenia may action in bisected of the cases and appears to be the aftereffect of atomic assuming of the platelet glycoprotein (GP)-IIb/IIIa receptor by the HIV-GP 160/120 antigen. Decreased platelet assembly is accepted in HIV infection behindhand of the platelet count, and it may be associated with the ultrastructural accident in HIV-infected megakaryocytes.

Anemia may be present in as abounding as 20% of patients at the time of diagnosis, and it occurs in as abounding as 80% of patients at some point. Patients with analytic AIDS are added acceptable than others to accept anemia, as are patients with low CD4+ counts.

The analysis is apparently multifactorial in best patients. Accepted accidental factors are cartilage bottom suppression, iatrogenic causes, vitamin deficiencies, suppressed erythropoietin production, and a blunted erythropoietin response. Cartilage bottom aggression with lymphoma or Kaposi bump may be noted. Cartilage bottom abolishment may be due to bacilli such as MAC, parvovirus B19, or CMV. Disseminated fungemia can annual anemia.

Neutropenia is empiric in 10% of patients with aboriginal asymptomatic HIV infections and in 50% of patients with AIDS. Neutropenia after-effects from the above mechanisms, as able-bodied as from medication. Granulocyte-macrophage colony-stimulating agency (GM-CSF) and G-CSF deficiencies not abandoned abate neutrophil assembly but additionally abate granulocytic and monocytic function. GM-CSF and G-CSF advance added neutrophilic function, including superoxide production, phagocytosis, intracellular killing, and antibody-dependent cellular cytotoxicity.

Neurologic effects

HIV exhibits tropism for the CNS, abnormally the microglia. As abounding as 10% of accouchement with AIDS accept accelerating encephalopathy, and the cerebrospinal aqueous (CSF) viral amount is activated with cerebral dysfunction. Accelerating white amount decline and academician decline may develop. Neurologic affection advance forth with adorning delay.

Viral resistance

In agreement of the mechanisms of attrition development, the accelerated about-face amount and aerial absurdity amount of about-face transcriptase induces 3300 fresh distinct mutations per day. Back a alteration improves the adaptation of the virus in an absolute biologic environment, that quasispecies is called to reproduce. The college the viral amount and the college the amount of replication, the greater the cardinal of aggressive quasispecies.

Approximately 10-15% of fresh infections are multidrug aggressive in adults. Drug-resistant quasispecies can be transmitted to a fetus or neonate.

HIV attrition develops because of low antiretroviral biologic (ARD) levels due to several factors including variations in biologic assimilation and metabolism and contravention because of adverse furnishings or a poor compassionate of the accent of the medication. Viral altar sites may be apparent to low levels of ARDs, and aggressive quasispecies may develop.

Etiology

Infection is due to HIV, a circuitous affiliate of the Lentivirus brand of the Retroviridae family. HIV-1 is the best accepted annual of HIV infection in the Americas, in Europe, in Asia, and in Africa. HIV-2 has acquired epidemics in West Africa, although this virus is additionally begin in European countries. HIV-2 ache progresses added boring than HIV-1 disease, and HIV-2 is beneath catching than HIV-1.

HIV-1 subtypes alter by geographic region. HIV-1 subtype B is absolute in the United States. Non-B subtypes are decidedly accustomed in Africa and Asia. The aerial manual amount from Africa to Europe has added the assortment of subtypes in Europe. Non-B subtype HIV-1 infections are accretion in the United States.

Vertical manual of HIV from mother to boyish is the capital avenue by which adolescence HIV infection is acquired; the accident of perinatal accretion is 25%. African epidemiologic abstracts of about 2000 breed announce that changeable breed may be added afflicted to HIV infection afore bearing and continuing afterwards bearing compared with macho infants.

Epidemiology

United States statistics

The HIV seroprevalence amount in abundant women is as aerial as 0.3%. The seroprevalence of women adulterated with HIV is accomplished in the Northeast, followed by the South. Perinatal HIV manual ante are 25% but as low as 2% in basic women with viral endless of beneath than 100 copies/mL.

Although antibacterial interventions accept bargain vertical transmissions, cases of perinatal HIV manual abide to occur. This is abundantly because of absent opportunities for prevention, decidedly amid women who abridgement prenatal affliction or who are not actuality offered autonomous HIV counseling and testing during pregnancy. In abounding as 40% of the mothers of breed with perinatally acquired HIV infection, the HIV infection was not accepted afore delivery.

The CDC estimates that in 2009, in the 40 states with arcane name-based HIV infection reporting, an estimated 131 breed acquired HIV infection by agency of vertical (mother-to-infant) transmission. Estimates abode the aiguille of perinatally-transmitted HIV in the US at 1651 cases in 1991.

The CDC estimates that in 2009, in those 40 states, the cardinal of pediatric HIV infections diagnosed was as follows :

Under age 13 years: 166

Ages 13-14 years: 21

Ages 15-19 years: 2036

In 2009, 12 cases of perinatally transmitted backward HIV ache (AIDS) were diagnosed; 8,640 accumulative estimated perinatally transmitted AIDS cases were diagnosed through 2009.

At the end of 2008, 3022 accouchement boyish than 13 years were active with HIV infection in the 40 states with arcane name-based HIV infection reporting.

In the absolute United States in 2009, an estimated 13 cases of AIDS were diagnosed in accouchement boyish than 13 years. The accumulative estimated cardinal of diagnoses of AIDS in accouchement boyish than 13 years through 2009 in the United States is 9448.

In the United States, the cardinal of fresh cases of pediatric AIDS is decreasing, mostly because of accessible bloom initiatives apropos accepted HIV testing for abundant women and use of zidovudine in adulterated abundant women and their bairn infants.

In 2007, 19 US accouchement boyish than 15 years died of HIV disease. These numbers are in abrupt adverse to what is occurring internationally.

International statistics

The WHO estimates that over 33 actor individuals are adulterated with HIV worldwide, and 90% of them are in developing countries. HIV has adulterated 4.4 actor accouchement and has resulted in the deaths of 3.2 million. Each day, 1800 children—the all-inclusive majority newborns—are adulterated with HIV. About 7% of the citizenry in sub-Saharan Africa is adulterated with HIV; these individuals represent 64% of the world's HIV-infected population. Furthermore, 76% of all women adulterated with HIV alive in this region.

HIV-1 is the best accepted annual of HIV infection in the Americas, in Europe, in Asia, and in Africa. HIV-1 subtypes alter by geographic region. HIV-1 subtype B is absolute in the United States, admitting non-B subtype HIV-1 infections are increasing.

The HIV seroprevalence amount amid abundant women in South America is 0.3-5%; in sub-Saharan Africa, the ambit is 13-45%. In Europe, the HIV seroprevalence is greatest in western countries; France, Spain, and Italy accept the accomplished incidences. Abundant women in burghal areas of these countries accept a seroprevalence amount as aerial as 1%.

Although the anniversary cardinal of fresh HIV infections has been steadily crumbling back the backward 1990s, the epidemics in Eastern Europe and in Central Asia abide to grow; the cardinal of bodies active with HIV in these regions accomplished an estimated 1.6 actor in 2005—an admission of about 20-fold in beneath than 10 years. The cutting majority of these bodies active with HIV are young; 75% of infections appear amid 2000 and 2004 were in bodies boyish than 30 years. In Western Europe, the agnate allotment was 33%.

The consequence of the AIDS catching in Asia is significant. Although civic HIV infection levels are low in Asia compared with added continents (notably Africa), the populations of abounding Asian nations are so ample that alike low prevalences reflect ample numbers of bodies are active with HIV. The seroprevalence amount in abundant women is already 2%, and the vertical manual amount is 24% afterwards breastfeeding. Indian mothers adulterated with HIV commonly breastfeed and accept manual ante as aerial as 48%.

Perinatal manual ante are about low in Europe and aerial in Africa, absolute of treatment. Basic women affect 13% and 40% of accouchement in Europe and Africa, respectively. The amount of postnatal manual in Africa and added developing countries is animated because of the charge to breastfeed.

HIV-1 is the best accepted annual of HIV infection in the Americas, Europe, Asia, and Africa. HIV blazon 2 (HIV-2) has acquired epidemics in West Africa, admitting this virus is additionally begin in European countries. HIV-1 subtypes alter by geographic region. Non-B subtypes are decidedly accustomed in Africa and in Asia. The aerial manual amount from Africa to Europe has added the assortment of subtypes in Europe.

Globally, accouchement alfresco the United States are not faring as well. Every day, 1400 accouchement become HIV absolute and 1000 accouchement die of HIV-related causes. An estimated 2.5 actor accouchement accepted boyish than 15 years are active with HIV/AIDS. In sub-Saharan Africa alone, 1.9 actor accouchement are active with HIV/AIDS and added than 60% of all fresh HIV infections action in women, infants, or boyish children. As of 2007, 90% of the anew adulterated accouchement are breed who admission HIV from their adulterated mothers. Alarmingly, 90% of babies who admission the ache from adulterated mothers are begin in sub-Saharan Africa. The prevalence of HIV infection amid angular accouchement has been estimated to be as aerial as 25%.

The prevalence of HIV infection in Asia and Europe varies appreciably because of assorted cultural practices and abridgement of a civic advertisement arrangement in abounding areas. The bartering sex artisan industry in countries such as Thailand and in the Caribbean Islands is amenable for added HIV manual to boyish girls and, vertically, to infants.

In 2004, added than bisected a actor accouchement boyish than 15 years died from HIV/AIDS. In 2006, this cardinal decreased to 380,000. In 2002, HIV/AIDS was the seventh arch annual of bloodshed in accouchement in developing countries. The ache progresses rapidly in about 10-20% of accouchement who are infected, and they die of AIDS by age 4 years, admitting 80-90% survive to a beggarly age of 9-10 years.

In afflicted regions of sub-Saharan Africa, the baby bloodshed amount has added by 75% due, in part, to the orphaned cachet of best children. In adverse to abundant of the developed world, the bloodshed ante for accouchement boyish than 5 years are college today than in 1990 in abounding African countries, mostly because of the adverse furnishings of HIV/AIDS.

A 2006 South African abstraction estimated that HIV/AIDS is the distinct better annual of baby and adolescence deaths in rural South Africa. HIV/AIDS is now amenable for 332,000 boyish deaths in sub-Saharan Africa, about 8% of all boyish deaths in the region.

Racial differences in incidence

Black and Hispanic accouchement are disproportionately affected. As of 2002, HIV infection was the 7th and 10th arch annual of afterlife in atramentous accouchement and in Hispanic teens, respectively. About 62% of accouchement with AIDS are black.

In the United States, accouchement from boyhood communities accept been best afflicted by AIDS. Added than 50% of afflicted accouchement are black, and hardly beneath than 25% are Hispanic. Of the fresh adolescence HIV cases in 2003, 68% occurred in African Americans. The cardinal of pediatric AIDS cases appear in atramentous non-Hispanic accouchement is 3.4 times college than in white non-Hispanic accouchement and is 2.6 times college than that of Hispanic children.

Sexual differences in incidence

Women of bearing age are one of the fastest growing groups with AIDS; 20% of AIDS cases in adults action in this group.

Young bodies (aged 15-44 y) annual for one of the fastest growing adulterated groups and annual for about bisected of all infections. Amid boyish people, boyish women are added acceptable to become infected. In sub-Saharan Africa, added than two thirds of all adolescence adulterated are boyish girls. Variations in frequencies in the sexes in added regions of the apple depend on the advantage of bartering sex workers and the admeasurement of a brief and adaptable workforce added acceptable to be afar from family.

Age-related differences in incidence

Because vertical manual from mother to boyish is the capital avenue by which pediatric HIV infection is acquired, best accouchement who are HIV absolute should be articular in infancy. Although accepted analysis strategies can anticipate vertical transmission, the drugs are artlessly not accessible in abounding places, abnormally in Africa.

Nevertheless, the age of presentation can be awful capricious in a high-risk boyish who was ahead unidentified. Accouchement can be asymptomatic for abounding years, and the actualization of an adept infection in a 10-year-old boyish or in an boyish in whom AIDS is afterwards diagnosed is not rare. Accouchement who admission HIV by agency of nonvertical manual may accept an affliction during the astute appearance of the retroviral syndrome, or they may present abounding years afterwards with adept or alternate infections.

The CDC estimates that 50% of all fresh HIV infections in the United States action amid individuals age-old 13-24 years. This is an important accomplishment that influences the bloodshed ante in boyish adults. For example, HIV is the 5th arch annual of afterlife amid atramentous women age-old 20-24 years, and it is the arch annual of bloodshed in atramentous women age-old 25-34 years.

Prognosis

Although HIV infection is usually baleful in children, abnormally in developing countries, the development of fresh antiretroviral drugs is promising. The abridgement of admission to antiretroviral agents by accouchement in developing countries is of accurate concern.

The comestible cachet of the boyish and the activity with which viral archetype is controlled are ascendant in free the aftereffect of best accouchement with HIV disease.

Aggressive analysis of adept infections prevents the added deleterious furnishings of accessory ache from avant-garde and added abrasion the patient. The amusing ambience and the stressors to which accouchement are apparent accept additionally been affiliated to the progression of the disease.

Hematologic disturbances, such as anemia, thrombocytopenia, and neutropenia, admission the accident of complications and death. Resolution of anemia improves the prognosis, and analysis of anemia with erythropoietin improves survival. Neutropenia decidedly increases the accident of bacterial infection, and analysis of neutropenia with granulocyte colony-stimulating agency essentially decreases the accident of bacteremia and death.

Infection with Mycobacteriumavium circuitous (MAC) hastens death, abnormally in patients with circumstantial anemia (defined as a hematocrit < 25%).

The afterward factors are associated with rapidly accelerating ache in infants:

Avant-garde affectionate disease

Aerial affectionate viral load

Low affectionate CD4+ count

Prematurity

In utero transmission

Aerial viral amount in the aboriginal 2 months of life

Abridgement of acrid antibodies

Attendance of p24 antigen

AIDS-defining illnesses

Aboriginal cytomegalovirus (CMV) infection

Aboriginal neurologic disease

Abortion to thrive

Early-onset diarrhea

Each logarithmic abatement in the viral amount afterwards the alpha of analysis decreases the accident of progression by 54%.

Baseline CD4+ T-lymphocyte allotment and associated abiding accident of afterlife in HIV-infected accouchement is as follows :

< 5%: 97%

5-9%: 76%

10-14%: 43%

15-19%: 44%

20-24%: 25%

25-29%: 31%

30-34%: 10%

≥35%: 33%

Baseline HIV RNA archetype cardinal (copies/mL) and associated abiding accident for afterlife in HIV-infected accouchement is as follows :

Undetectable (ie, ≤4,000): 24%

4,001-50,000: 28%

50,001- 100,000: 15%

100,001- 500,000: 40%

500,001-1,000,00: 40%

1,000,000: 71%

The accustomed progression of angular acquired HIV infection appears to accept a trimodal distribution. About 15% of accouchement accept rapidly accelerating disease, and the butt has either a abiding accelerating advance or an infection arrangement archetypal of that empiric in adults. Beggarly adaptation is about 10 years.

In resource-poor nations, the progression to afterlife accelerates. In some instances, abutting to 45-90% of HIV-infected accouchement died by the age of 3 years. However, amid accouchement and adolescents, the alpha of aggregate analysis including protease inhibitors reduces the accident of afterlife by an estimated 67%. Also, host analysis comedy an important role in HIV-1–related ache progression and neurologic impairment

The patient's all-embracing progression and cast is followed up by application the CDC allocation arrangement for accouchement adulterated with HIV (see Staging).

Patient Education

Educating parents apropos the accent of acquiescence with assigned medications and bloom affliction visits is a above claiming because of abounding factors. See Deterrence/Prevention for added altercation about this topic.

Patients should be accomplished apropos the manual of HIV. Accretion their acquaintance of the apparatus and after-effects of HIV manual is important. Safe amusing interactions that do not betrayal bodies to an added accident for HIV manual should additionally be emphasized.

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Measles Clinical Presentation

History

The patient history is notable for exposure to the virus. The incubation period from exposure to onset of measles symptoms ranges from 7 to 14 days (average, 10-12 days). Patients are contagious from 1-2 days before the onset of symptoms. Healthy children are also contagious during the period from 3-5 days before the appearance of the rash to 4 days after the onset of rash. On the other hand, immunocompromised individuals can be contagious during the duration of the illness. 

The first sign of measles is usually a high fever (often >104^o F [40^o C]) that typically lasts 4-7 days. This prodromal phase is marked by malaise, fever, anorexia, and the classic triad of conjunctivitis (see the image below), cough, and coryza (the “3 Cs”). Other possible associated symptoms include photophobia, periorbital edema, and myalgias.

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Measles conjunctivitis The characteristic enanthem generally appears 2-4 days after the onset of the prodrome and lasts 3-5 days. Small spots (Koplik spots) can be seen inside the cheeks during this early stage (see the image below).

Koplik spots in measles. Photograph courtesy of World Health Organization. The exanthem usually appears 1-2 days after the appearance of Koplik spots; mild pruritus may be associated. On average, the rash develops about 14 days after exposure, starting on the face and upper neck (see the image below) and spreading to the extremities. Immunocompromised patients may not develop a rash.
Child with measles. Photograph courtesy of Centers for Disease Control and Prevention. The entire course of uncomplicated measles, from late prodrome to resolution of fever and rash, is 7-10 days. Cough may be the final symptom to appear.

Modified and atypical measles

Modified measles is a milder form of measles that occurs in individuals who have received serum immunoglobulin after their exposure to the measles virus. Similar but milder symptoms and signs may still occur, but the incubation period may be as long as 21 days.
Atypical measles occurs in individuals who were vaccinated with the original killed-virus measles vaccine between 1963 and 1967 and who have incomplete immunity. After exposure to the measles virus, a mild or subclinical prodrome of fever, headache, abdominal pain, and myalgias precedes a rash that begins on the hands and feet and spreads centripetally. The eruption is accentuated in the skin folds and may be macular, vesicular, petechial, or urticarial. The live-attenuated vaccine replaced the killed vaccine in 1967 and is not associated with atypical measles.

Physical Examination

Enanthem

 

Near the end of the prodrome, Koplik spots (ie, bluish-gray specks or “grains of sand” on a red base) appear on the buccal mucosa opposite the second molars (see the image below).

 

Enanthem of measles (Koplik spots) The Koplik spots generally are first seen 1-2 days before the appearance of the rash and last until 2 days after the rash appears. This enanthem begins to slough as the rash appears. Although this is the pathognomonic enanthem of measles, its absence does not exclude the diagnosis.

Exanthem

Blanching, erythematous macules and papules begin on the face at the hairline, on the sides of the neck, and behind the ears (see the images below). Within 48 hours, they coalesce into patches and plaques that spread cephalocaudally to the trunk and extremities, including the palms and soles, while beginning to regress cephalocaudally, starting from the head and neck. Lesion density is greatest above the shoulders, where macular lesions may coalesce. The eruption may also be petechial or ecchymotic in nature.
Face of boy with measles Morbilliform rash Patients appear most ill during the first or second day of the rash. The exanthem lasts for 5-7 days before fading into coppery brown hyperpigmented patches, which then desquamate. The rash may be absent in patients with underlying deficiencies in cellular immunity.

Complications

Most complications of measles occur because the measles virus suppresses the host’s immune responses, resulting in a reactivation of latent infections or superinfection by a bacterial pathogen. Consequently, pneumonia, whether due to the measles virus itself, to tuberculosis, to or another bacterial etiology, is the most frequent complication. Pleural effusion, hilar lymphadenopathy, hepatosplenomegaly, hyperesthesia, and paresthesia may also be noted. 

 

Complications of measles are more likely to occur in persons younger than 5 years or older than 20 years, and complication rates are increased in persons with immune deficiency disorders, malnutrition, vitamin A deficiency, and inadequate vaccination. Immunocompromised children and adults are at increased risk for severe infections and superinfections.
Common infectious complications include otitis media, interstitial pneumonitis,^[19] bronchopneumonia, laryngotracheobronchitis (ie, croup), exacerbation of tuberculosis, transient loss of hypersensitivity reaction to tuberculin skin test, encephalomyelitis, diarrhea, sinusitis, stomatitis, subclinical hepatitis, lymphadenitis, and keratitis, which can lead to blindness. In fact, measles remains a common cause of blindness in many developing countries.
Rare complications include hemorrhagic measles, purpura fulminans, hepatitis, disseminated intravascular coagulation (DIC), subacute sclerosing panencephalitis (SSPE), thrombocytopenia, appendicitis, ileocolitis, pericarditis, myocarditis, acute pancreatitis,^[20] and hypocalcemia.^[21] Transient hepatitis may occur during an acute infection.
Approximately 1 of every 1,000 patients develops acute encephalitis, which often results in permanent brain damage and is fatal in about 10% of patients. In children with lymphoid malignant diseases, delayed-acute measles encephalitis may develop 1-6 months after the acute infection and is generally fatal.
An even rarer complication is SSPE, a degenerative CNS disease that can result from a persistent measles infection. SSPE is characterized by the onset of behavioral and intellectual deterioration and seizures years after an acute infection (the mean incubation period for SSPE is approximately 10.8 years).
The complications of measles in the pregnant mother include pneumonitis, hepatitis, subacute sclerosing panencephalitis, premature labor, spontaneous abortion, and preterm birth of the fetus. Perinatal transmission rates are low

References

1. Sabella C. Measles: not just a childhood rash. Cleve Clin J Med. Mar 2010;77(3):207-13. [Medline].
2. [Guideline] Centers for Disease Control and Prevention. Recommended immunization schedules for persons aged 0 through 18 years---United States, 2009. CDC Recommended Vaccine Schedule. Dec 2008;57(51;52):[Full Text].
3. Meissner HC, Strebel PM, Orenstein WA. Measles vaccines and the potential for worldwide eradication of measles. Pediatrics. 2004;114(4):1065-9. [Medline]. [Full Text].
4. Smeeth L, Cook C, Fombonne E, et al. MMR vaccination and pervasive developmental disorders: a case-control study. Lancet. 2004;11-17;364(9438):963-9. [Medline].
5. Schneider-Schaulies S, Schneider-Schaulies J. Measles virus-induced immunosuppression. Curr Top Microbiol Immunol. 2009;330:243-69. [Medline].
6. Markowitz LE, Preblud SR, Fine PE, Orenstein WA. Duration of live measles vaccine-induced immunity. Pediatr Infect Dis J. Feb 1990;9(2):101-10. [Medline].
7. Reported vaccine-preventable diseases--United States, 1993, and the childhood immunization initiative. MMWR Morb Mortal Wkly Rep. Feb 4 1994;43(4):57-60. [Medline].
8. Orenstein WA, Papania MJ, Wharton ME. Measles elimination in the United States. J Infect Dis. May 1 2004;189 Suppl 1:S1-3. [Medline].
9. Coleman KP, Markey PG. Measles transmission in immunized and partially immunized air travellers. Epidemiol Infect. Jul 2010;138(7):1012-5. [Medline].

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Measles

Measles, also known as rubeola, is one of the most contagious infectious diseases, with at least a 90% secondary infection rate in susceptible domestic contacts. It can affect people of all ages, despite being considered primarily a childhood illness. Measles is marked by prodromal fever, cough, coryza, conjunctivitis, and pathognomonic enanthem (ie, Koplik spots), followed by an erythematous maculopapular rash on the third to seventh day. Infection confers life-long immunity.


A generalized immunosuppression that follows acute measles frequently predisposes patients to bacterial otitis media and bronchopneumonia. In approximately 0.1% of cases, measles causes acute encephalitis. Subacute sclerosing panencephalitis (SSPE) is a rare chronic degenerative disease that occurs several years after measles infection.

After an effective measles vaccine was introduced in 1963, the incidence of measles decreased significantly. Nevertheless, measles remains a common disease in certain regions and continues to account for nearly 50% of the 1.6 million deaths caused each year by vaccine-preventable childhood diseases. The incidence of measles in the United States and worldwide is increasing, with outbreaks being reported particularly in populations with low vaccination rates.
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Maternal antibodies play a significant role in protection against infection in infants younger than 1 year and may interfere with live-attenuated measles vaccination. A single dose of measles vaccine administered to a child older than 12 months induces protective immunity in 95% of recipients. Because measles virus is highly contagious, a 5% susceptible population is sufficient to sustain periodic outbreaks in otherwise highly vaccinated populations.


A second dose of vaccine, now recommended for all school-aged children in the United States,[2] induces immunity in about 95% of the 5% who do not respond to the first dose. Slight genotypic variation in recently circulating strains has not affected the protective efficacy of live-attenuated measles vaccines.

Unsubstantiated claims that suggest an association between the measles vaccine and autism have resulted in reduced vaccine use and contributed to a recent resurgence of measles in countries where immunization rates have fallen to below the level needed to maintain herd immunity.


Considering that for industrialized countries such as the United States, endemic transmission of measles may be reestablished if measles immunity falls to less than 93-95%, efforts to ensure high immunization rates among people in both developed and developing countries must be sustained.


Supportive care is normally all that is required for patients with measles. Vitamin A supplementation during acute measles significantly reduces risks of morbidity and mortality.


For patient education resources, see Bacterial and Viral Infections, as well as Measles and Skin Rashes in Children
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Etiology

The cause of measles is the measles virus, a single-stranded, negative-sense enveloped RNA virus of the genus Morbillivirus within the family Paramyxoviridae. Humans are the natural hosts of the virus; no animal reservoirs are known to exist. This highly contagious virus is spread by coughing and sneezing via close personal contact or direct contact with secretions.

Risk factors for measles virus infection include the following:

Children with immunodeficiency due to HIV or AIDS, leukemia, alkylating agents, or corticosteroid therapy, regardless of immunization status
Travel to areas where measles is endemic or contact with travelers to endemic areas
Infants who lose passive antibody before the age of routine immunization

Risk factors for severe measles and its complications include the following:

Malnutrition
Underlying immunodeficiency
Pregnancy
Vitamin A deficiency
Epidemiology
United States statistics


The practice of administering 2 doses of live-attenuated measles vaccine to children to prevent school outbreaks of measles was implemented when the vaccine was first licensed in 1963. The immunization program resulted in a decrease of more than 99% in reported incidence.


From 1989 to 1991, a major resurgence occurred, affecting primarily unvaccinated preschoolers. This measles resurgence resulted in 55,000 cases and 130 deaths[7] and prompted the recommendation that a second dose of measles vaccine be given to preschoolers in a mass vaccination campaign that led to the effective elimination in the United States of endemic transmission of the measles virus.[8]


By 1993, vaccination programs had interrupted the transmission of indigenous measles virus in the United States; since then, most reported cases of measles in the United States have been linked to international travel.[9] By 1997-1999, the incidence of measles had been reduced to a historic low (< 0.5 cases per million persons). From 1997 to 2004, the reported incidence was as low as 37-116 cases per year. From November 2002 on, measles was not considered an endemic disease in the United States.


From 2000 through 2007, an average of 63 cases were reported annually to the US Centers for Disease Control and Prevention (CDC). In 2004, 34 cases were reported; after that all-time low, however, the annual incidence began to increase, with most cases linked either directly or indirectly to international travel. Incomplete vaccination rates facilitate the spread once the virus is imported to the United States.


In 2005, 66 cases of measles were reported to the CDC.[10] Of these, 34 were linked with a single outbreak in Indiana associated with the return of an unvaccinated 17-year-old American traveling in Romania. In 2006, a total of 49 confirmed cases were reported in the United States.


From January to June 2008, 131 cases of measles were reported to the CDC.[11] Although 90% of those 131 cases were associated with importation of the virus to the United States from overseas, 91% of those affected were unvaccinated or had unknown or undocumented vaccination status. At least 47% of the 131 measles infections were in school-aged children whose parents chose not to have them vaccinated.[11]


In the period from January 1 to May 20, 2011, a total of 118 cases were reported to the CDC; this represents the highest reported number of measles cases for the same period since 1996.[12] Of the 118 cases, 105 (89%) were associated with importation; the source of the remaining 13 cases could not be ascertained. In all, 105 (89%) of the 118 patients were unvaccinated; 24 (20%) were persons 12 months to 19 years of age whose parents claimed a religious or personal exemption.


Approximately half of the 118 cases—58, or 49%—were accounted for by 9 outbreaks. The largest of these outbreaks involved 21 persons in Minnesota, in a setting where parental concerns about the safety of measles, mumps, and rubella (MMR) vaccine caused many children to go unvaccinated.[13] As a result of this outbreak, many persons were exposed, and at least 7 infants too young to receive MMR vaccine were infected.


Despite the highest recorded immunization rates in history, young children who are not appropriately vaccinated may experience more than a 60-fold increase in risk of disease due to exposure to imported measles cases from countries that have not yet eliminated the disease.
International statistics


In developing countries, measles affects 30 million children a year and causes 1 million deaths. Measles causes 15,000-60,000 cases of blindness per year.


In 1998, the cases of measles per 100,000 total population reported to the World Health Organization (WHO) was 1.6 in the Americas, 8.2 in Europe, 11.1 in the Eastern Mediterranean region, 4.2 in South East Asia, 5.0 in the Western Pacific region, and 61.7 in Africa. In 2006, only 187 confirmed cases were reported in the Western Hemisphere (mainly in Venezuela, Mexico, and the United States).[14]


Between 2000 and 2008, the number of worldwide measles cases reported to the WHO and the United Nations Children’s Fund (UNICEF) declined by 67% (from 852,937 to 278,358). During the same 8-year period, global measles mortality dropped by 78%. However, it is believed that global measles incidence and mortality remain underreported, with many countries, particularly those with the highest disease burden, lacking complete, reliable surveillance data.[15]


Since 2008, France has been experiencing an outbreak of measles, which has not yet begun to slacken.[16] Over the same period, outbreaks have also been occurring in the 46 countries of the WHO African Region.[17] Worldwide, most reported cases of measles continue to be from Africa.
Age-related demographics


Although measles is historically a disease of childhood, infection can occur in unvaccinated or partially vaccinated individuals of any age or in those with compromised immunity.


Unvaccinated young children are at the highest risk. Age-specific attack rates may be highest in susceptible infants younger than 12 months, school-aged children, or young adults, depending on local immunization practices and incidence of the disease. Complications such as otitis media, bronchopneumonia, laryngotracheobronchitis (ie, croup), and diarrhea are more common in young children.


Of the 66 cases of measles reported in the United States in 2005, 7 (10.6%) involved infants, 4 (6.1%) involved children aged 1-4 years, 33 (50%) involved persons aged 5-19 years, 7 (10.6%) involved adults aged 20-34 years, and 15 (22.7%) involved adults older than 35 years.[10]


Among the 118 US patients reported to have measles between January 1 and May 20, 2011, age ranged from 3 months to 68 years.[12] More than half were younger than 20 years: 18 (15%) were younger than 12 months, 24 (20%) were 1-4 years old, 23 (19%) were 5-19 years old, and 53 (45%) were 20 years of age or older.


In heavily populated, underdeveloped countries, measles is most common in children younger than 2 years.

Sex- and race-related demographics

Unvaccinated males and females are equally susceptible to infection by the measles virus. Excess mortality following acute measles has been observed among females at all ages, but it is most marked in adolescents and young adults. Excessive non–measles-related mortality has also been observed among female recipients of high-titer measles vaccines in Senegal, Guinea Bissau, and Haiti.[18]


Measles affects people of all races.

Prognosis

The prognosis for measles is generally good, with infection only occasionally being fatal. The CDC reports the childhood mortality rate from measles infection in the United States to be 0.1-0.2%. However, many complications and sequelae may develop (see Complications), and measles is a major cause of childhood blindness in developing countries.


Globally, measles remains one of the leading causes of death in young children. According to the CDC, measles caused an estimated 197,000 deaths worldwide in 2007.[14] An estimated 85% of these deaths occurred in Africa and Southeast Asia. From 2000-2007, deaths worldwide fell by 74% (to 197,000 from an estimated 750,000), thanks to the partnership of several global organizations.


Case-fatality rates are higher among children younger than 5 years. The highest fatality rates are among infants aged 4-12 months and in children who are immunocompromised because of human immunodeficiency virus (HIV) infection or other causes.


Complications of measles are more likely to occur in persons younger than 5 years or older than 20 years, and morbidity and mortality are increased in persons with immune deficiency disorders, malnutrition, vitamin A deficiency, and inadequate vaccination.


Croup, encephalitis, and pneumonia are the most common causes of death associated with measles. Measles encephalitis, a rare but serious complication, has a 10% mortality.

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Scarlet Fever

Scarlet Fever
Scarlet fever is an upper respiratory tract infection associated with a characteristic rash, which is caused by an infection with pyrogenic exotoxin (erythrogenic toxin)–producing Group A Streptococcus in individuals who do not have antitoxin antibodies. It is now encountered less commonly and is less virulent than in the past, but the incidence is cyclic, depending on the prevalence of toxin-producing strains and the immune status of the population. The modes of transmission, age distribution, and other epidemiologic features are otherwise similar to those for GAS pharyngitis.

It is characterized by:

• Sore throat
• Fever
• Bright red tongue with a "strawberry" appearance
• Characteristic rash, which:

• is fine, red, and rough-textured; it blanches upon pressure.
• appears 12–48 hours after the fever.
• generally starts on the chest, armpits, and behind the ears.
• spares the face (although some circumoral pallor is characteristic).
• is worse in the skin folds. These Pastia lines (where the rash runs together in the armpits and groin) appear and can persist after the rash is gone.
• may spread to cover the uvula.

The rash begins to fade three to four days after onset and desquamation (peeling) begins. "This phase begins with flakes peeling from the face. Peeling from the palms and around the fingers occurs about a week later. Peeling also occurs in axilla, groin, and tips of the fingers and toes


Rash:
The rash appears within 24–48 hr after onset of symptoms, although it may appear with the 1st signs of illness . It often begins around the neck and spreads over the trunk and extremities. It is a diffuse, finely papular, erythematous eruption producing a bright red discoloration of the skin, which blanches on pressure. It is often more intense along the creases of the elbows, axillae, and groin. The skin has a goose-pimple appearance and feels rough. The face is usually spared, although the cheeks may be erythematous with pallor around the mouth. After 3–4 days, the rash begins to fade and is followed by desquamation, 1st on the face, progressing downward, and often resembling that seen subsequent to a mild sunburn. Occasionally, sheetlike desquamation may occur around the free margins of the fingernails, the palms, and the soles.
Pharynx:
Examination of the pharynx of a patient with scarlet fever reveals essentially the same findings as with GAS pharyngitis.
Tongue:
In addition, the tongue is usually coated and the papillae are swollen. After desquamation, the reddened papillae are prominent, giving the tongue a strawberry appearance.


Diagnosis:
Typical scarlet fever is not difficult to diagnose; however, the milder form with equivocal pharyngeal findings can be confused with viral exanthems, Kawasaki disease, and drug eruptions. Staphylococcal infections are occasionally associated with a scarlatiniform rash. A history of recent exposure to a GAS infection is helpful. Identification of GAS in the pharynx confirms the diagnosis, if uncertain.
Treatment:
the treatment and course of scarlet fever are no different from those of any strep throat. In case of penicillin allergy, clindamycin or erythromycin can be used with success. Patients should no longer be infectious after taking antibiotics for 24 hours. People who have been exposed to scarlet fever should be watched carefully for a full week for symptoms, especially if aged 3 to young adult. It is very important to be tested (throat culture) and if positive, seek treatment.

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Poliomyelitis

Poliovirus infections with wild-type virus may follow 1 of several courses: inapparent infection, which occurs in 90–95% of cases and causes no disease and no sequelae; abortive poliomyelitis; nonparalytic poliomyelitis; or paralytic poliomyelitis. Paralysis, if it occurs, appears 3–8 days after the initial symptoms.

Incubation Period:

The incubation period of poliovirus from contact to initial clinical symptoms is usually considered to be 8–12 days, with a range of 5–35 days.

Abortive Poliomyelitis.

In about 5% of patients, a nonspecific influenza-like syndrome occurs 1–2 wk after infection, which is termed abortive poliomyelitis. Vomiting occurs irregularly. The physical examination may be normal or may reveal nonspecific pharyngitis, abdominal or muscular tenderness, and weakness.
Nonparalytic Poliomyelitis.
In about 1% of patients infected with wild-type poliovirus, signs of abortive poliomyelitis are present, as are more intense headache, nausea, and vomiting, as well as soreness and stiffness of the posterior muscles of the neck, trunk, and limbs. Fleeting paralysis of the bladder and constipation are frequent. Approximately ? of these children have a short symptom-free interlude between the 1st phase (minor illness) and the 2nd phase (CNS disease or major illness). Nuchal and spinal rigidity are the basis for the diagnosis of nonparalytic poliomyelitis during the 2nd phase.
Physical examination reveals nuchal-spinal signs and changes in superficial and deep reflexes. Gentle forward flexion of the occiput and neck will elicit nuchal rigidity. Head drop is demonstrated by placing the hands under the patient’s shoulders and raising the trunk. True nuchal rigidity will persist during this maneuver. In the early stages the reflexes are normally active and remain so unless paralysis supervenes. Changes in reflexes, either increased or decreased, may precede weakness by 12–24 hr. The superficial reflexes, the cremasteric and abdominal reflexes, and the reflexes of the spinal and gluteal muscles are usually the 1st to diminish. The spinal and gluteal reflexes may disappear before the abdominal and cremasteric reflexes. Changes in the deep tendon reflexes generally occur 8–24 hr after the superficial reflexes are depressed and indicate impending paresis of the extremities. Tendon reflexes are absent with paralysis. Sensory defects do not occur in poliomyelitis.
Paralytic Poliomyelitis.
Paralytic poliomyelitis develops in about 0.1% of persons infected with poliovirus, causing 3 clinically recognizable syndromes that represent a continuum of infection differentiated only by the portions of the CNS most severely affected.
These are (1) spinal paralytic poliomyelitis, (2) bulbar poliomyelitis, and (3) polioencephalitis.
Spinal paralytic poliomyelitis may occur as the 2nd phase of a biphasic illness, the 1st phase of which corresponds to abortive poliomyelitis. Severe muscle pain is present, and sensory and motor phenomena (e.g., paresthesia, hyperesthesia, fasciculations, and spasms) may develop. On physical examination the distribution of paralysis is characteristically spotty. Single muscles, multiple muscles, or groups of muscles may be involved in any pattern. Within 1–2 days, asymmetric flaccid paralysis or paresis occurs. Involvement of 1 leg is most common, followed by involvement of 1 arm. To detect mild muscular weakness, it is often necessary to apply gentle resistance in opposition to the muscle group being tested. Examination at this point may reveal nuchal stiffness or rigidity, muscle tenderness, initially hyperactive deep tendon reflexes (for a short period) followed by absent or diminished reflexes, and paresis or flaccid paralysis. In the spinal form there is weakness of some of the muscles of the neck, abdomen, trunk, diaphragm, thorax, or extremities. Sensation is intact; sensory disturbances, if present, suggest a disease other than poliomyelitis.


The paralytic phase of poliomyelitis is extremely variable; some patients progress during observation from paresis to paralysis, whereas others recover, which may be slow or rapid. The extent of paresis or paralysis is directly related to the extent of neuronal involvement; paralysis occurs if more than 50% of the neurons supplying the muscles are destroyed. Paralysis of the lower limbs is often accompanied by bowel and bladder dysfunction ranging from transient incontinence to paralysis with constipation and urinary retention.
The onset and course of paralysis are variable in developing countries. The biphasic course is rare and typically presents as a single phase in which prodromal symptoms and paralysis occur in a continuous fashion. In developing countries, where a history of intramuscular injections precedes paralytic poliomyelitis in about 50–60% of patients, patients may present initially with fever and paralysis (provocation paralysis). Occasionally spasm and increased muscle tone with a transient increase in deep tendon reflexes occur in some patients, whereas in most patients flaccid paralysis occurs abruptly. Once the temperature returns to normal, progression of paralytic manifestations stops. Lack of improvement from paralysis within the 1st several weeks or months after onset is usually evidence of permanent paralysis.
Bulbar poliomyelitis may occur as a clinical entity without apparent involvement of the spinal cord. Infection is a continuum, and designation of the disease as bulbar implies only dominance of the clinical manifestations by dysfunctions of the cranial nerves and medullary centers. The clinical findings seen with bulbar poliomyelitis with respiratory difficulty (other than paralysis of extraocular, facial, and masticatory muscles) include (1) nasal twang to the voice or cry caused by palatal and pharyngeal weakness (hard-consonant words such as “cookie” or “candy” bring this out best); (2) inability to swallow smoothly, resulting in accumulation of saliva in the pharynx, indicating partial immobility (holding the larynx lightly and asking the patient to swallow will confirm such immobility); (3) accumulated pharyngeal secretions, which may cause irregular respirations that appear interrupted and abnormal even to the point of falsely simulating intercostal or diaphragmatic weakness; (4) absence of effective coughing, shown by constant fatiguing efforts to clear the throat; (5) nasal regurgitation of saliva and fluids as a result of palatal paralysis, with inability to separate the oropharynx from the nasopharynx during swallowing; (6) deviation of the palate, uvula, or tongue; (7) involvement of vital centers in the medulla, which manifest as irregularities in rate, depth, and rhythm of respiration; as cardiovascular alterations, including blood pressure changes (especially increased blood pressure), alternate flushing and mottling of the skin, and cardiac arrhythmias; and as rapid changes in body temperature; (8) paralysis of 1 or both vocal cords, causing hoarseness, aphonia, and ulti mately asphyxia unless this is recognized by laryngoscopy and managed by immediate tracheostomy; and (9) the rope sign, an acute angulation between the chin and larynx caused by weakness of the hyoid muscles (the hyoid bone is pulled posteriorly, narrowing the hypopharyngeal inlet).
Uncommonly, bulbar disease may culminate in an ascending paralysis (Landry type), in which there is progression cephalad from initial involvement of the lower extremities. This kind of bulbar disease may be rapidly fatal.
The course of bulbar disease is variable; some patients die as a result of extensive, severe involvement of the various centers in the medulla; others recover partially but require ongoing respiratory support, and others recover completely. Cranial nerve involvement is seldom permanent. Atrophy of muscles may be evident, patients immobilized for long periods may develop pneumonia, and renal stones may form as a result of hypercalcemia and hypercalciuria secondary to bone resorption.
Seizures, coma, and spastic paralysis with increased reflexes may be observed. Irritability, disorientation, drowsiness, and coarse tremors are often present with peripheral or cranial nerve paralysis that coexists or ensues. Paralytic poliomyelitis with ventilatory insufficiency results from several components acting together to produce ventilatory insufficiency resulting in hypoxia and hypercapnia. Because respiratory insufficiency may develop rapidly, close continued clinical evaluation is essential. Despite weakness of the respiratory muscles, the patient may respond with so much respiratory effort associated with anxiety and fear that overventilation may occur at the outset, resulting in respiratory alkalosis. Such effort is fatiguing and contributes to respiratory failure.
Pure spinal poliomyelitis with respiratory insufficiency involves tightness, weakness, or paralysis of the respiratory muscles (chiefly the diaphragm and intercostals) without discernible clinical involvement of the cranial nerves or vital centers that control respiration, circulation, and body temperature. The cervical and thoracic spinal cord segments are chiefly affected. Pure bulbar poliomyelitis involves paralysis of the motor cranial nerve nuclei with or without involvement of the vital centers. Involvement of the 9th, 10th, and 12th cranial nerves results in paralysis of the pharynx, tongue, and larynx with consequent airway obstruction. Bulbospinal poliomyelitis with respiratory insufficiency affects the respiratory muscles and results in coexisting bulbar paralysis.


The clinical findings associated with involvement of the respiratory muscles include (1) anxious expression; (2) inability to speak without frequent pauses, resulting in short, jerky, “breathless” sentences; (3) increased respiratory rate; (4) movement of the ala nasi and of the accessory muscles of respiration; (5) inability to cough or sniff with full depth; (6) paradoxical abdominal movements caused by diaphragmatic immobility due to spasm or weakness of 1 or both leaves; and (7) relative immobility of the intercostal spaces, which may be segmental, unilateral, or bilateral. When the arms are weak, and especially when deltoid paralysis occurs, there may be impending respiratory paralysis because the phrenic nerve nuclei are in adjacent areas of the spinal cord. Observation of the patient’s capacity for thoracic breathing while the abdominal muscles are splinted manually indicates minor degrees of paresis.

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