Bacterial
Protozoa
Syphilis Gonorrhea Chancroid
Trichomoniasis
Viral AIDS HSV Warts
Is a systemic and highly infectious STD that usually begins with mucous membrane and quickly becomes systemic
a.k.a LUES VENERA CAUSATIVE AGENT: Treponema pallidum – spirochete
Treponema pallidum Has no other host but man Believed that mo will pass thru mucosa w/o a visible crack Does not withstand drying Has been found alive in a glass for ½ hour after a glass was rinsed by cold water Can not be grown in vitro
MOT: Direct Contact- infectious exudates from obvious or concealed moist early lesions of skin and mucous membrane, body fluids and secretions
Blood Transfusion Transplacental Transfer
syphilis
neonatorum
Indirect Contact Health Professionals developed primary lesions on hands after examination of infectious lesions
INCUBATION PERIOD: 2 to 6 weeks POC: Variable and Indefinite SUSCEPTIBILITY: Universal No natural immunity OCCURRENCE: Widespread Primarily involving young persons between 15 – 34 yrs More prevalent in urban than rural areas M>F High prevalence among male homosexuals
Pathogenesis Entry of MO Organism multiplies and locally disseminate systematically through the blood stream STAGES OF SYPHILIS: PRIMARY SYPHILIS SECONDARY SYPHILIS TERTIARY SYPHILIS
Pathogenesis Microorganism penetrates skin/mucosa Multiplies in subcutaneous tissue at the site of entry Proliferation of immune cells (lymphocytes /antibodies) Inflammatory response leading to ulceration or wearing away of tissue
STAGES:
PRIMARY SYPHILIS 1. Sites of Primary Lesions Anogenital region Extragenital area – lips, tongue, tonsil, finger, nipple
2. Description of primary lesion (hard chancre) Chancre begins at the site of inoculation Appears like a pimple if it is on skin
Begins as a single painless papule that rapidly becomes eroded and usually becomes indurated with a characteristic cartilaginous consistency on palpation of the edge and base of the ulcer.
PRIMARY SYPHILIS Chancre Inguinal lymphadenopathy Lesions become multiple painful vesicles, which later ulcerate Fever
COURSE: Lesion heals within 4 – 6 weeks without treatment (chancre in men)
It doesn’t mean that it is cured!!!
B. SECONDARY SYPHILIS OCCURRENCE: Approximately 6 – 7 weeks after primary lesions appear. Development of mucocutaneous lesions and generalized lymphadenopathy GENERAL S/ SXS: Fever Malaise Sore Throat Weight Loss Anorexia
Nausea Constipation Headache, muscle and joint pain fever
Skin Hair Lymphatic system Mucous membrane
Pathogenesis Microorganism migrates into the lymphatics To blood stream throughout the body Lesions/Lymphadenopathy/microorganism can be found anywhere in
the body ”GREAT IMITATOR” Basilar meningitis
CN deficits, AGN, hepatitis and synovitis
B. SECONDARY SYPHILIS
SKIN Anogenital are Mouth Axilla Toe webs Soles of feet Palms of hands Initially: bilaterally symmetric pink non pruritic round macules
B. SECONDARY SYPHILIS
SKIN Non pruritic round macule that appears b/w rolls of fat and Transforms into papular follicular pustular lesions -become enlarged and eroded -produces broad, moist, pink or gray – white, highly infectious lesions called
CONDYLOMATA LATA
-develop in warm, moist body areas common in labia, anus, corners of the mouth
B. SECONDARY SYPHILIS CONDYLOMATA LATA This 45-year-old house maid suffered from multiple moist grayish papules on the vulva for a month. Dark field microscopy showed spirochetes consistent with Treponema pallidum and her syphilis serology (VDRL) was reactive with a titer of 1:256. She was treated with benzathine penicillin 2.4 million units intramuscularly in each buttocks. All cutaneous lesions had resolved 3 weeks later when she returned for reevaluation.
multiple confluent moist grayish-white papules
B. SECONDARY SYPHILIS
CONDYLOMATA LATA
B. SECONDARY SYPHILIS
HAIR “Moth – eaten scalp” – alopecia beginning on the occipital area Loss of eyelashes, beard and lateral 1/3 of the eyebrows. temporary
MUCOUS MEMBRANE mucous patches of the mouth, throat and cervix Yellow to white in color and covered with exudates, which when removed reveals a soft glistening appearance.
LYMPHATIC SYSTEM
generalized non-tender lymphadonapathy w/ occasional splenomegal
Secondary syphilis: moth-eaten alopecia, which affects the scalp, eyebrows, eyelashes, and beard. (Courtesy of Stacy Smith, M.D.)
Secondary syphilis: alopecia of the eyebrows. This patient presented to the dermatologist with the sole complaint of loss of eyebrow hair.
B. SECONDARY SYPHILIS
COURSE: lesions slowly fade away, but may recur during the latent phase LATENT SYPHILIS- no clinical s/sx but with reactive serological test - 2/3 are asymptomatic until death -immune system controls infection
-
Patients who were remained untreated/ destructive but non-infectious
OCCURRENCE: May begin as early as 1 year after the initial infection. Typically occurs after a latent period of 5 – 20 years Systemic infection
C. TERTIARY SYPHILIS
LESIONS: Cardiovascular syphilis Arteritis of the aorta—vessel necrosis– dilatation of the ao aortic regurgitation—CHF Syphilitic Aortitis Multiple small infarcts—direct damage to neural cells in SC and cerebral cortex Arteritis Neurosyphilis/CNS paresis., personality changes, slurred speech, Meningeal syphilis tremors, resembles CVA Meningovascular syphilis Tabes dorsalis-
dorsal root ganglia, demyelination of posterior columns
- ataxic, loss of position sense, vibratory, deep pain, temperature, sensation, impotence, loss of bladder or bowel function.
C. TERTIARY SYPHILIS “Benign” tertiary syphilis Gummas or indolent ulcers of the skin and mucous membranes Periostitis of the tibia, clavicle, skull and other bones Gummas of the liver Induration and atrophy of the base of the tongue
osteochondritis of femur and tibia
C. TERTIARY SYPHILIS “Benign” tertiary syphilis
Granulomas connective tissue in the form of small grainy particles along with masses of tiny blood vessels that forms over wound
DIAGNOSIS: 3.Gross Appearance of the Lesion 2. Dark Field Microscopy of Exudate - from skin scrapings/test not readily - confirms the diagnosis of syphilis in secondary
available primary and
3. Serology -VDRL slide test -Rapid Plasma Reagin ( RPR) 4. Fluorescent Treponemal Antibody Absorption test
TREATMENT: 1. Penicillin 2.4 mu or more (benzathine penicillin G)- IM 2-4 mu/week x 3 weeks ****allergy to penicillin – tetracycline
and doxycycline
2. Screen and treat all sexual partners (CONTACT TRACING)
If client tests positive, provide counseling in privacy. Teach about disease and treatment. Provide emotional support. UNIVERSAL PRECAUTION Keep lesion dry and dispose drainage properly Abstain from sexual contact atleast 1 month after the treatment Encourage pt to undergo VDRL after 3, 6, 12, 24 months
-Aka Jack, Clap, Gleet, Dose, Strai, Drips, Morning drop -GONOCOCCAL INFECTION OF THE GENITOURINARY TRACT - INVOLVES THE MUCOSAL LINING OF GUT,RECTUM, PHARYNX
Causative agent: Neisseria gonorrhoeae -Highly contagious -Gram (-) found in pairs -Fragile and doesn’t survive long outside the body -Killed by drying, UV, ordinary disinfectant
OCCURRENCE: •Common worldwide •M=F •practically all ages •Common among promiscuous male, homosexuals, younger adult groups.
MOT: Primarily by sexual intercourse Rarely by indirect contact of genital secretions with other mucous membranes Direct contact with vaginal secretions (opthalmic neonatorum) INCUBATION PERIOD: 2 – 7 Days, sometimes longer POC: •Months if untreated, especially in untreated aymptomatic Female •Specific therapy usually ends communicability within hours except from infections with penicillin – resistant strain
INCIDENCE IS INCREASING DUE TO: Short Incubation Period High promotion of asymptomatic carriers Development of strains resistant to Penicillin and Tetracyclines Changing sexual habits Revised morals standards DIAGNOSTICS: Gram’s Staining, Nucleic Acid Probe Test, Direct Fluorescent Antibody
Pathogenesis Infection Gonococci become adherent to the urethral epithelium Penetration of the mucosa and elicits an acute inflammatory response consisting of leukocytes Edema of the gland ducts or plugs of debris obstructs drainage to form abscess Infection can spread to mucosal surfaces like fallopian tube, endometrium, peritoneal cavity of women Scarring from abscess/ tubal involvement Stricture/narrowing of fallopian tube Decreased ovarian egg flow Sterility
GONOCOCCAL INFECTIONS IN FEMALES: 3.Cervicitis 4.Vaginitis 5.Anorectal Gonorrhea 6.Pharyngeal Gonorrhea 1. Cervicitis With yellow or green mucopurulent discharge Dysuria, Urinary frequency, (1st) Cervical erythema, red swollen vulva, abN menses,
Early s/sx of pelvic infxn (fever, N/V, abd’s pain/tenderness) Primarily affects the cervical os Complication of PID: Endometritis Salpingitis Tubal infertility
GONOCOCCAL INFECTIONS IN FEMALES:
2. Vaginitis Occurs commonly in prepubertal and postmenopausal women Abundant purulent discharge Red and edematous vaginal mucosa
GONOCOCCAL INFECTIONS IN FEMALES:
3. Anorectal Gonorrhea Anorectal pain or pruritus Tenesmus Rectal bleeding Purulent rectal discharge
4. Pharyngeal Gonorrhea Fellatio Cervical Lymphadenopathy Tonsillar enlargement, possibly exudates Complications: Salphingitis--- PID--- infertility (scarring and occlusion of the FT)
GONOCOCCAL INFECTIONS IN MALES:
1.Acute Urethritis -
most common manifestation Inflammation can cause stricture that prevents passage of Urine
2. Urethral Discharge Discharge is mucoid and scant initially but becomes profuse and purulent within two days
3. Dysuria with urinary frequency and urgency Complications: rectal infection (homosexuals), epidymitis, and prostatitis(pelvic pain and fever)
Diagnostic 1. Gram’s staining 2. Nucleic Acid Probe Test 3. Direct Fluorescent Antibody Test * males- gram stain (culture smear) * females- pap smear, specimen taken from cervix/anal canal
TREATMENT: 2.Ceftriaxone 250 mg IM(SD) plus Doxycycline 100 mg BIDX 7 Days 2. Quinolones 3. Spectinomycin x 7 days
FOLLOW UP: Cultures – 14 days after completion of treatment Serology (VDRL) – should be drawn at time of initial treatment and at monthly intervals.
NURSING CONSIDERATIONS: If client tests positive, provide counseling in private. Teach about prevention and control. Provide emotional support. Case finding Contact tracing Safe sex(abstinence, condom, monogamous relationship) Crede’s prophylaxis
ULCUS MOLLE, SOFT CHANCRE, SOFT SORE CAUSATIVE AGENT:
Haemophilus ducreyi
TRANSMISSION: Direct sexual contact with discharges from open lesions INCUBATION PERIOD: 4 to 7 days
PERIOD OF COMMUNICABILITY: As long as the infectious agent persists in the original lesion or discharging regional lymph nodes usually until healed OCCURRENCE: Common in tropical and subtropical regions, especially in seaports.
APPEARANCE: Initial Lesion: Papular with surrounding Erythema, pustules produce multiple painful, irregular and deep genital ulcers
After 2 to 3 days: papules evolve into pustules which spontaneously ruptures and forms a sharply circumscribed ulcer that is not indurated, ulcers are painful and bleed easily
APPEARANCE: ulcers are painful and bleed easily
APPEARANCE: Other signs: Inguinal adenitis and suppuration
DIAGNOSIS: 1. 2. 3. 4.
PE Rule out genital herpes, primary syphilis Smear and Culture Biopsy and darkfield examination
TREATMENT: 3.Ceftriaxone 250 mg IM x 1 dose 4.Azithromycin 1 gm PO x 1 dose 5.Erythromycin 500 mg PO x 7 days 6.Ciprofloxacin 500 mg PO BID x 3 days
NURSING MANAGEMENT: Practice Standard Precaution Check for drug allergy Instruct patient to abstain from sexual contact until healing is complete Wash genitalia with soap and water
Viral AIDS HSV Warts
AIDS
AIDS Acquired Immunodeficiency Syndrome/ Acquired Immune-Deficiency Syndrome - is a human disease characterized by progressive destruction of the body's immune system.
AGENT: Human Immunodeficiency Virus -1 and -2 (HIV -1 and HIV – 2) - “slow virus” long incubation period (7-12 yrs)
AIDS •Originated from Eastern Africa thru precursor virus of a chimpanzee •Not hereditary or inborn •Affects CD4+ T = Lymphocytes decreasing the body’s immune response(increase susceptibility to infection) •Antibodies develop in 2 weeks to 6 months •May remain asymptomatic for several years
AIDS OCCURRENCE: Worldwide (Pandemic) TRANSMISSION: 6. Homosexual and Heterosexual Contact 7. By blood and Blood Products 8. Infected Mothers to Infants
AIDS HIV (dendritic cells in the mucosa of the genital tract) Transported to the lymph nodes HIV infects lymphocytes Systemic infection Body’s immune response Antibodies(cytotoxic t-cells) Specific for HIV infected cells Viremia level decreased to a “plateau level” When HIV infection takes place, Anti-HIV bodies are produced but they do not appear immediately WINDOW EFFECT In some cases, antibodies to HIV become detectable 4-6 weeks after infection HIV in circulation, it invades several types of cells (lymphocytes, macrophages, langehans cell
AIDS HIV attacks immune system, microorganism attaches to CHON molecule called CD4 which is found in the surface of T- cells Once the virus enters the T4, it inserts its genetic materials into the T4’s nucleus taking over the cell to replicate itself T4 cell dies after being used by HIV for replication Virus mutates rapidly making it difficult for the body to “recognize” the invaders Reverse transcriptase which copy information for virus to replicate
HALLMARK: progressive decreased in CD4 T cells
AIDS STAGES OF AIDS Acute HIV Syndrome Clinical Latency Symptomatic disease
AIDS STAGES OF AIDS Acute HIV Syndrome ( 3 - 6 weeks after Primary Infection) General: MINOR : fever pharyngitis LAD headache arthralgias myalgias lethargy malaise anorexia weight loss nausea vomiting diarrhea
AIDS STAGES OF AIDS Acute HIV Syndrome Neurologic: meningitis encephalitis peripheral neuropathy myelopathy Dermatologic: erythematous maculopapular rash mucocutaneous ulceration
AIDS MAJOR: Weight loss: 10% of body weight Chronic diarrhea for more than a month Prolonged fever for 1 month AIDS: Adult: 2 major and 1 minor Pedia: 2 major and 2 minor
AIDS STAGES OF AIDS Clinical Latency may last up to 10 years Progressive decline of Immunodeficiency
CD4+ T – Cells
AIDS STAGES OF AIDS Symptomatic Disease Respiratory: Acute Bronchitis, Sinusitis, PCP Cardiovascular: HIV – associated cardiomyopathy GIT: Thrush, Oral hairy leukoplakia, aphthous ulcers GUT: HIV – associated nephropathy Neurological: Kaposi’s sarcoma, AIDS Dementia Complex
AIDS STAGES OF AIDS Symptomatic Disease Pulmonary Opportunistic infections 1. PCP 2. Histoplasmosis 3. TB GIT 1. 2. 3. 4.
Mycobacterium avium CMV Hepatitis B, C, D HIV-wasting syndrome
AIDS STAGES OF AIDS Symptomatic Disease GIT 5. Oral Candidiasis 6. Oral hairy leukoplakia
AIDS STAGES OF AIDS Symptomatic Disease Gynecologic A. Vaginal Candidiasis CNS AIDS Dementia syndrome - progressive cognitive and function
deterioration
motor
AIDS STAGES OF AIDS Symptomatic Disease Kaposi’s Sarcoma - vascular malignancy - red to purple, palpable, non-blanching, painless lesion - usually on face, penis, scrotum Treatment: Chemotherapy
AIDS DIAGNOSTIC PROCEDURE: 4.ELISA -Serological test for antibodies against HIV; reactive test -Standard screening test but less reliable in early stage -Results usually appear after 22-27 days 2. Western Blot -Confirmatory dxtic test -More accurate than ELISA -If ELISA 2x (+); western blot is recommended -Done during late stage/ can detect lower levels of antibodies 3. PCR test- for viral nucleic acid sequences to assess levels of viremia 4. CD4-T-cell- less than 200 cells/mm3
AIDS TREATMENT: 3.No cure. Counseling after positive diagnosis. 2. Medications: A. Nucleoside Analogue Reverse transcriptase Inhibitor - slows disease process by inhibiting reverse transcriptase enzyme Zidovudine (AZT) Didanosine Zalcitabine Stavudine Lamivudine
AIDS 2. Medications: B. Non-nucleoside reverse transcriptase inhibitor Delavirdine Nevirapine Efavirenz C. Protease inhibitor - prevents assembly of viral particles Ritonavir Saquinavir Indinavir Nelfinavir
AIDS NURSING CONSIDERATIONS: 3.Wear gloves, wash hands whenever handling blood or body fluids. (PPE) 4.Follow universal precautions. 5.Teach preventive measures. A. Latex condom use B. No needle sharing
AIDS NURSING CONSIDERATIONS: 4. Teach about disease process. 5. Provide emotional support. 6. Screen sexual partners. 7. Blood spills should be cleaned immediately using common household disinfectant (bleach) 8. Label blood specimens with “AIDS precaution”
AGENT: Herpes Simplex Virus (HSV) *occurs primarily below waist STD TRANSMISSION: Type 2 Virus – Sexual Contact * Can spread by touching an unaffected part of the body after touching herpes lesion INCUBATION PERIOD: 2 – 12 Days POC: Patients with primary genital lesions are infective for about 7 – 12 days; with recurrent disease for 4 days to a week.
MANIFESTATIONS: Fever
Headache
Malaise
Myalgia
Pain
itching
Dysuria
inguinal LAD Vaginal and urethral discharge
Lesions: widely spaced bilateral vesiculopustular or painful erythematous ulcers.
Diagnostics: 2. Viral culture 3. Direct immunofluorescence staining of vesicular exudates 4. Pap smear
TREATMENT: symptomatic and supportive ** chronic disease w/o cure; prevent/ lessen occurrences and giving palliative
Relieve vulvar pain- keep the area clean and dry; wear lose fitting non-synthetic undergarments; sitz bath; cooling applications and analgesic meds Acyclovir - to reduce healing time - (not recommended during pregnancy)
NURSING CONSIDERATIONS: •Teach patients to use warm compresses or take sitz bath several times a day. •Use a drying agent, such as povidone iodine solution. •Increase fluid intake. •Avoid all sexual contact during the active phase. •Those with Herpetic Whitlow – instruct not to share towels or eating utensils. - Abstain from direct patient care.
DIGITAL HERPES SIMPLEX The herpes simplex virus infection on the finger is known as herpetic whitlow. Grouped, fluid-filled or pus-filled, blisters are typical and usually itch and/or are painful.
WARTS – VERRUCA VULGARIS (VENEREAL WARTS) GENITAL WARTS - Benign growth that typically occur in multiple, painless, clusters on the vagina, vulva, cervix, perineum, anorectal area, urethral meatus/ glans penis Condyloma acuminatum
cauliflower shaped lesions that appear on moist skin surfaces such as the vagina and anus
CAUSATIVE AGENT: Human Papilloma Virus (HPV) TRANSMISSION: Direct contact , Sexually transmitted INCUBATION PERIOD: 3 to 4 months average, Ranges from 1 month to 2 years
PERIOD OF COMMUNICABILITY: Unknown, but probably as long as visible S/Sx No symptoms Itchiness occurs with anogenital warts DIAGNOSTIC EXAM: •Pap Smear and Visualization, •Hybrid Capture Assay •Application of 5% acetic acid
lesions persists
TREATMENT: 3.Cryosurgery – with liquid nitrogen 4.Electrocautery- burning 5.Laser-small warts 6.Fluorouracil- antineoplastic 7.Acid solution ( Podophyllin cream) 8.Trichloroacetic acid 9.Screen sexual partners NURSING CONSIDERATIONS: 3.If client tests positive, provide counseling in privacy. 4.Teach about disease. 5.Provide emotional support.
Protozoa Trichomoniasis
Trichomoniasis A PROTOZOAL INFECTION CAUSING VULVOVAGINITIS
CAUSATIVE AGENT: Trichomonas vaginalis – inhabits the lower genital tract of females (moist environments) and at the urethra and prostate of males
Trichomoniasis TRANSMISSION: By contact with vaginal and urethral discharges of infected persons during sexual intercourse. Possibly by direct contact with contaminated articles such as wet towels and swimsuits, washcloths and douching equipment. INCUBATION PERIOD: 5 to 28 Days
Trichomoniasis PERIOD OF COMMUNICABILITY: For the duration of the infection SUSCEPTIBILITY/ RESISTANCE: General but clinical disease is mainly on females.
Trichomoniasis
Trichomoniasis
Trichomoniasis DIAGNOSTICS: 3.Microscopy of wet mounts of secretions 5.Direct immunofluorescent antibody staining
Trichomoniasis TREATMENT: 3.Metronidazole (Flagyl) 2 grams once daily 5.Treat sexual partner.
Trichomoniasis NURSING CONSIDERATIONS: 3.Teach to avoid intercourse after treatment until both partners are cured. 4.Teach to avoid alcohol while taking metronidazole (acts like Antabuse and alcohol). 5.Provide counseling in privacy. 6.Teach about disease. 7.Teach to practice scrupulous cleanliness.