Infectious Disease - Adult 2 PDF

Infectious Disease Adult 2 Jessica Dong, DNP, FNP-BC Cellulitis Cellulitis Cellulitis is divided into two categories of purulent and non-purulent types Non-intact skin acts as a portal of entry S/S superficial localized swelling, erythema, pain, and warmth to the area involved and freque...

Infectious Disease Adult 2 Jessica Dong, DNP, FNP-BC Cellulitis Cellulitis Cellulitis is divided into two categories of purulent and non-purulent types Non-intact skin acts as a portal of entry S/S superficial localized swelling, erythema, pain, and warmth to the area involved and frequently produce pus, induration, and pain. May be associated with systemic symptoms such as fevers, chills, and malaise Cellulitis can involve the deeper dermis and subcutaneous fat, spreading rapidly and extending deep from the dermis to the subcutaneous tissue Leg is a very common site Common Causes of Cellulitis Group A β-hemolytic streptococci Staphylococcus aureus may be implicated in purulent forms of cellulitis Other pathogens may also be implicated in cellulitis when cellulitis occurs as a complication of animal bites, with injuries occurred in freshwater or salt­water, or in immunocompromised hosts Community-acquired MRSA can cause skin infections Ask patient about penetrating trauma. Assess sites of injections, surgical sites, indwelling catheters, or preexisting open wounds Purulent Abscesses are collections of pus that may be within the dermis or deeper layers  painful or tender to palpation  appear as raised lesions that may be fluctuant, red, and/or nodular  often a central pustule with erythematous margins  skin abscesses are polymicrobial infections, consisting of bacteria from local skin flora and the adjacent mucous membranes  Staph. aureus  Community-acquired MRSA Furuncles (boils) are infections that arise at the hair follicle and extend deep into the dermis, where an abscess forms A carbuncle forms when several adjacent furuncles coalesce, forming an inflammatory mass with pus draining from multiple follicles Nonpurulent Diagnosis is largely by clinical recognition May be streptococci (but may also be staphylococcal) If no obvious culturable source is present, empirical treatment should be pursued Causal pathogen may be determined by culturing any existing vesicular fluid, pus, ulcer, or erosions Blood cultures should be obtained if there is extensive body surface involvement, underlying comorbidities including immunodeficiencies, previous splenectomy, diabetes, lymphedema, malignancy, neutropenia, specific exposures such as animal bites or water-associated injuries, and recurrent or refractory cellulitis  Mild illness in an immune competent host can be treated outpatient Moderate Severe purulent drainage along with patients who are considered systemic involvement severe are defined as those hospitalization refractory to oral antibiotics refractory to incision and drainage demonstrating hemodynamic alteration who are immunocompromised hospitalization  Treatment Mild cellulitis Antibiotics effective against streptococci and staphylococci should be used.  Penicillin, amoxicillin, amoxicillin-clavulanate, penicillinase-resistant penicillin such as dicloxacillin, a cephalosporin such as cephalexin, or clindamycin (5-7 day course) Treatment may be extended if symptoms have not resolved within that time (14 days) Renal and/or hepatic impairment: adjust dose as needed Uncomplicated cases of nonulcerative cellulitis in patients with diabetes can be treated with amoxicillin-clavulanate or quinolones (ciprofloxacin, levofloxacin)  These antibiotics are chosen because they cover gram-negative organisms and anaerobes that may infect patients with diabetes. More severe ulcerative infections or cases of osteomyelitis require intravenous (IV) antibiotics and consultation with a surgeon for debridement. https://www.uptodate.com/contents/cellulitis-and-skin-abscess-in-adults-treatment  Treatment Moderate or severe purulent Systemic antibiotics that primarily target S. aureus are required If the patient has failed initial non-MRSA antibiotic treatment, is critically ill, has had previous MRSA infections, or is known to be MRSA colonized, empirical antibiotics should target MRSA pending culture and susceptibility results If the patient can take oral therapy, possible antibiotics for MRSA (methicillin- resistant Staphylococcus aureus) include  trimethoprim-sulfamethoxazole (TMP- SMX) or  doxycycline plus Amoxicillin Possible antibiotics for MSSA (methicillin- sensitive Staphylococcus aureus) include penicillinase-resistant penicillin such as dicloxacillin Treat according to the full laboratory-reported susceptibilities https://www.uptodate.com/contents/cellulitis-and-skin-abscess-in-adults-treatment Treatment In purulent skin and soft tissue infections (SSTIs), incision and drainage is key to treatment. Small furuncles often spontaneously drain with the application of moist heat Larger furuncles, carbuncles, and skin abscesses may require incision and drainage with a focus on adequate debridement NSAIDs Postural drainage Herpes Simplex Herpes Simplex HSV-1, usually oral infection. HSV-2, usually genital infections. Both HSV-1 and HSV-2 are DNA viruses No seasonal variation, no known animal vectors Infected individuals lack clinical manifestations of infection and can shed the virus in the absence of symptoms Transmission of HSV occurs by direct contact with active lesions or with secretions containing the virus HSV may enter the host through a skin or intact mucous membranes The virus attaches itself to epithelial cells, enters, and replicates, exploiting cellular components. Once infected, cells die and release clear fluid, causing the formation of vesicles, which can fuse to form multinucleated giant cells During the infection process, the virus gains access to and infects regional, sensory, or autonomic nerves The virus travels through the nerve axon to the ganglion, where it establishes a latent infection. The virus can reactivate and travel down the axon, where it causes a recurrent infection in the cutaneous area innervated by the affected root Herpes Simplex Phases HSV infection has three distinct phases: Primary: Usually the most severe and may start after an incubation period of 2 to 14 days, can be as high as 26 days Genital lesions are often painful, with an average duration of symptoms of 22 to 28 days Patients frequently report a prodrome of burning or tenderness at the site Multiple painful round vesicles then appear at the site of infection and may be accompanied by tender lymphadenopathy in regional nodes Fever, dysuria, discharge, or malaise may accompany the primary infection. Ulceration subsequently occurs, and lesions crust over and heal in immunocompetent patients within 2 to 3 weeks Latent: the virus remains dormant in the ganglion of the nerve that serves the affected dermatome Recurrent: infection characterized by virus reactivation and the reappearance of lesions in the dermatome affected during the primary infection. Reactivation of either HSV type can be caused by local or systemic stimuli, such as immunodeficiency, trauma to mucosa, stress, depression, chronic anxiety, and poor sleep recurrent infections tend to be shorter and usually less severe, with markedly fewer lesions Assessment Elicit any history of HSV infection, HIV infection, or pregnancy Assess sexual history, partners Diagnosis Diagnosis of HSV infection can be made clinically with a thorough history and physical examination. However, laboratory confirmation should be considered in patients with a newly diagnosed primary infection The definitive test for the diagnosis of cutaneous herpes simplex infections remains Herpes viral culture Polymerase chain reaction (PCR) assay are extremely sensitive. HSV PCR is a single test that both detects the presence of HSV DNA and determines which type is present in the positive samples HerpeSelect HSV-2 enzyme-linked immunosorbent assays (ELISA): Enzyme- linked immunosorbent assay (ELISA) for the qualitative detection of human IgG class antibodies to HSV-2 Treatment Most cases of mild herpes labialis are self-limiting and do not require treatment The only over-the-counter treatment approved by the FDA is docosanol (Abreva) Topical medications: Penciclovir cream (Denavir) is applied at the first sign of symptoms and every 2 hours (while awake) for 4 days. Xerese (acyclovir/hydrocortisone topical) is applied 5 times a day for 5 days.  Patients should be instructed to avoid products with salicylic acid, which can erode the compromised skin. Pain and discomfort can be treated with applications of over-the- counter analgesics or anesthetics such as camphor, benzyl alcohol, pramoxine, phenol, menthol, tetracaine, or benzocaine Protectants including petroleum jelly, lip balms, calamine, zinc oxide, allantoin, and cocoa butter may also be used Treatment Continued Recommended that therapy is extended longer if indicated by incomplete healing despite treatment Scabies Scabies Scabies typically is a poorly defined pruritic eruption often with linear burrows in the web spaces of the fingers. The scabies mite, Sarcoptes scabiei, is not visible to the unaided human eye Scabies is a contagious infection usually transmitted by direct, prolonged skin-to-skin contact with an infested person, commonly through sexual contact or sharing a bed with an infected individual Can affect the young and old Scabies is more prevalent in hot, humid environments as well as in low socioeconomic conditions and overcrowded areas The diagnosis is confirmed by scraping of a burrow and microscopic identification of mites, eggs, or feces Review of Systems and Physical Exam Patient will complain of itching which is a hypersensitivity reaction to the mites. Itching may be very intense at night S/s usually begin 2 to 4 weeks after infection in a person who was not previously sensitized. The mite can survive off the human host for up to 3 days Common burrow sites are the interdigital spaces of the hands, flexures of the wrists and arms, genitals, feet, buttocks, and axillae Assess for eczematous changes from nocturnal scratching and rubbing Assess for skin lesions: lesions at the site of infestation and lesions secondary to hypersensitivity to the mite. Small papules on an erythematous base form a disseminated tract near the waist, genitalia, breasts, buttocks, axillary folds, interdigital spaces, and wrists Intraepidermal burrows are linear or serpiginous (“spreading”) ridges and are produced by the infesting female mite The head, palms, and soles are usually spared in adults Assess if patient lives in crowded living conditions, an institutional facility such as nursing homes, prison, long-term care facilities, or if they work in a day care center Diagnoses and Treatment Definitive confirmation is made with a “scabies prep”: A drop of mineral oil is placed on a burrow, and the lesion is scraped or shaved. The sample is viewed under a microscope The “adhesive tape test”: Adhesive tape is adhered to the affected area, then rapidly removed. The tape is then applied to a slide and examined under a microscope Preferred initial therapy: Topical application of 5% permethrin cream (Elimite), should be left on for 8 to 12 hours and then washed off. The treatment must be repeated after 7 to 14 days Oral ivermectin therapy: 200 mcg/kg single oral dose followed by a repeat dose after 1-2 weeks Alternative: Benzyl benzoate lotion (10% to 25%) can be applied each night for 2 days in a row with reapplication at 7 days Important Considerations Identify and treat all household contacts Patients should be instructed to wash all clothing and bedding in hot water and dry on the hot cycle Vacuum stuffed sofas and chairs. Materials that cannot be washed should be placed in a plastic bag for 1 week or dry cleaned Patients should be educated that symptoms may continue to be present for 2 weeks after treatment. Have patients compile a list of personal or household contacts from the past 30 days for evaluation and treatment HIV/AIDS Fast Facts HIV/AIDS 10 yrs. is the median onset between HIV infection & AIDS CD4 T-lymphyocytes (Normal CD4 count 500 & 1500) AIDS by definition is a CD4 count < 200 along w/ some types of opportunistic infections or malignancies  Oral candidiasis  Fever, weight loss, diarrhea, cough, SOB  Kaposi’s sarcoma (purple to bluish-red bumps on skin)  Pneumocystis jirovecii (formerly P. carinii) infection can lead to death AIDS is the outcome of chronic HIV infection and consequent depletion of CD4 cells. It is defined as a CD4 cell count100,000 copies/ml (blood & genital secretions) Initial immune response could mimic mononucleosis symptoms… Symptoms seen in 50-90% within 2-4 weeks of HIV infection Fever Headache Sore throat Lymphadenopathy Rash Arthralgias & myalgias Mononucleosis Acute HIV continued During the initial infection antibodies may be negative 97% will develop antibodies within 3 months PCR can detect infection 7-28 days post exposure HIV-1 is the most common in strain globally (other than West Africa) West Africa: HIV-2 is the most common: HIV-2 is increasing in India Approximately 15 % of HIV infected persons in U.S. are unaware that they are infected HIV Risk Factors Sexual intercourse w/ an HIV infected person Sexual intercourse w/ gay or bisexual men Received blood products between 1975 until March 1985 History of illicit drug use History of other STDs Multiple partners Homeless Prisoners/jails HIV Diagnostic Testing CDC 4th generation testing Step 1: order HIV 1/HIV 2 & P24 antigen (combination antigen/antibody assay) w/ reflexes  During the first few weeks of infection, the amount of virus (viral load) and the p24 antigen level in the blood can be very high (remember antigens stimulate an immune response)  “Reflex” means that if + lab will automatically perform the follow-up tests to confirm results Step 2: If +, the lab will perform HIV-1, HIV-2 antibody differentiation immunoassay  This will confirm the result of the initial combination assay  Detects if infection is from HIV 1, HIV 2 or both viruses If indeterminate: order HIV RNA PCR ELISA: Older screening test, if positive the next step is Western blot test Western Blot test: Older test used for confirmation. If positive the next step is the HIV RNA PCR test HIV Diagnostic Testing Cont’d HIV RNA PCR detects HIV-1 RNA (actual viral presence) Order to test infants, if HIV + mother (New York State requires that all newborn babies be tested for HIV through the Newborn Screening Program) Order if HIV-1/HIV-2 antibody differentiation test is indeterminate Test can detect HIV infection as early as 7-28 days after exposure NOTE: To detect HIV-2, HIV-2-specific antibody and/or HIV-2 RNA testing should be performed HIV Viral Load Definition: Number of HIV RNA copies in 1 ml of plasma The more HIV there is in the blood (higher the viral load), then the faster CD4 cell count will fall and the greater the risk of becoming ill Test measures actively replicating HIV virus, progression of disease, & response to antiretroviral treatment Best sign of successful treatment is an undetectable viral load (fewer than 50 copies of HIV per milliliter of blood) If suspect acute or early HIV infection, order combination antigen/antibody immunoassay w/ viral load test HIV CD4 T-Cell Counts CD4 T-Cell Counts Normal 500-1500 cells/ml Two uses of CD4 counts: 1. stage HIV infection 2. determine ART (antiretroviral therapy) response If CD4 count rises w/decrease in viral load means patient is responding to ART (immune system improving) Values will vary throughout the day Test same time/day using the same laboratory each time CD4 is remeasured HIV Opportunistic Infection Toxoplasma gondii Infections (protozoa)- CNS infection CD4 count