utigutimicro

26

Microbial Diseases of the Urinary and Reproductive Systems

Microbial Diseases of the Urinary and Reproductive Systems Microbes usually enter the urinary system through

the urethra. Microbes usually enter the reproductive system

through the vagina (in females) or urethra (in males).

FEMALE URINARY ORGANS

Figure 26.1

FEMALE REPRODUCTIVE ORGANS

Figure 26.2a

MALE REPRODUCTIVE & URINARY ORGANS

Figure 26.3

NORMAL MICROBIOTA

Urinary bladder and upper urinary tract sterile

Lactobacilli predominant in the vagina >1,000 bacteria/ml or 100 coliforms/ml of

urine indicates infection

CYSTITIS Usually caused by E. coli S. saprophyticus May also be caused by

ProteusKlebsiellaEnterococcusPseudomonas

E. coli usually causes pyelonephritis. Antibiotic-sensitivity tests may be required before

treatment.

UTIUreteritis =

inflammation of ureter (maybe caused by stone in the ureter)

Cystitis = inflammation of bladder (caused by ascending bacterial infection usually E. coli)

Urethritis = inflammation of urethra (may lead to prostatitis and epididymitis)

“BAD STROKE”

FACTORS THAT CONTRIBUTE TO UTI

FEMALE (PROXIMITY TO THE ANUS, SHORTER URETHRA)

POOR HYGIENEUNSAFE SEXUAL PRACTICESBACK TO FRONT STROKEHIGH pH URINARY STASISKIDNEY STONESOBSTRUCTION OF URINE OUTFLOW

S/Sx:PAIN assessmentPain during and after urination =

cystitisPain after urination = urethritis Inguinal pain = ureteritisFlank pain = pyelonephritis Inflammatory manifestations

fever and chillsCx:Ascending infectionObstruction (stones/calculi)

http://images.google.com.ph/imgres?imgurl=http://www.alaska.net/~akdm/Images/UTI.GIF&imgrefurl=http://www.alaska.net/~akdm/Clinical/patient_ed/uti_pat_ed.htm&h=941&w=556&sz=9&hl=tl&start=17&tbnid=rxT8cWoXLWcXFM:&tbnh=148&tbnw=87&prev=/images?q=urinary+tract+infection&ndsp=18&svnum=10&hl=tl&lr=&sa=N

MANAGEMENT E. coli (most common C.A.) Increase fluids Warm sitz bath EMPTY the bladder Good hygiene Observe safe sexual

practice Front to back stroke Acidify urine (cranberry

juice, prune, plums) C/S test before giving

antibiotics For urosepsis give

aminoglycosides Observe complications

LEPTOSPIROSIS Leptospira interrogans Reservoir: Dogs and rats Transmitted by

skin/mucosal contact from urine-contaminated water

Diagnosis: Isolating bacteria or serological tests

Figure 26.4

Silver Stain of Leptospira interrogans serotype icterohaemorrhagiae

Obligate aerobes Characteristic hooked ends (like a

question mark, thus the species epithet – interrogans)

Leptospirosis Clinical Syndromes

Mild virus-like syndrome (Anicteric leptospirosis) Systemic with aseptic

meningitis (Icteric leptospirosis) Overwhelming disease (Weil’s

disease) Vascular collapseThrombocytopeniaHemorrhageHepatic and renal dysfunction

NOTE: Icteric refers to jaundice (yellowing of skin and mucus membranes by deposition of bile) and liver involvement

Leptospirosis, also called Weil’s disease in humans Direct invasion and replication in tissues Characterized by an acute febrile jaundice & immune

complex glomerulonephritis Incubation period usually 10-12 days with flu-like illness

usually progressing through two clinical stages:i. Leptospiremia develops rapidly after infection (usually lasts

about 7 days) without local lesionii. Infects the kidneys and organisms are shed in the urine

(leptospiruria) with renal failure and death not uncommon Hepatic injury & meningeal irritation is common

Pathogenesis of Icteric Leptospirosis

Clinical Progression of Icteric (Weil’s Disease) and Anicteric Leptospirosis

(pigmented part of eye)

Epidemiology of Leptospirosis

Mainly a zoonotic disease • Transmitted to humans from a variety of wild and domesticated

animal hosts• In USA most common reservoirs rodents (rats), dogs, farm

animals and wild animals Transmitted through breaks in the skin or intact mucus

membranes Indirect contact (soil, water, feed) with infected urine

from an animal with leptospiruria Occupational disease of animal handling

Comparison of Diagnostic Tests for Leptospirosis

SEXUALLY TRANSMITTED DISEASES (STDS )

Prevented by condoms Treated with antibiotics

GONORRHEA

Figure 26.5a

GONORRHEA Neisseria gonorrhoeae

Attaches to oral or urogenital mucosa by fimbriae.

Females may be asymptomatic; males have painful

urination and pus discharge.

Treatment is with antibiotics.

If left untreated, may result in

Endocarditis

Meningitis

Arthritis

Ophthalmia neonatorum

GONORRHEA

Figure 26.7

GONORRHEA

UN 26.1

NONGONOCOCCAL URETHRITIS

Chlamydia trachomatis May be transmitted to a newborn's eyes Painful urination and watery discharge

Mycoplasma hominis Ureaplasma urealyticum

PELVIC INFLAMMATORY DISEASE N. gonorrhoeae C. trachomatis Can block uterine tubes Chronic abdominal pain

GONORRHEA

Neisseria gonorrhea, gram (+)

IP: 3-7 days

28Rex Karl S. Teoxon, R.N, M.D

SIGNS AND SYMPTOMS

Females: usually asymptomatic or minimal urethral discharge w/ lower abdominal pain

Male: Mucopurulent discharge, Painful urination


GONORRHEAMANIFESTATIONS IN MEN

UrethritisEpididymitisProctitisPharyngitis

GONORRHEACLINICAL PRESENTATION

GONORRHEAMANIFESTATIONS IN WOMEN

UrethritisEndocervicitisProctitisPIDPharyngitis

GONORRHEADISSEMINATED INFECTION

ArthritisDermatitisPericarditis and endocarditis

MeningitisPerihepatitis

DISSEMINATED GONORRHEACLINICAL PRESENTATION

DIAGNOSIS

GSCS of cervical secretions on Thayer Martin medium


GONORRHEAGRAM STAIN

GONORRHEADIAGNOSIS

Clinical examinationGram stainCultureNucleic acid probes

MANAGEMENT

Ceftriaxone (Rocephin) 250 mg IM Ofloxacin (Floxin) 400 mg orally treat concurrently with Doxycycline or

Azithromycin for 50% infected w/ Chlamydia


GONORRHEASEQUELAE

InfertilityEctopic pregnancyChronic pelvic pain

COMPLICATION

PID ectopic pregnancy and infertility Peritonitis Perihepatitis Ophthalmia neonatorum Sepsis Arthritis


GONORRHEATREATMENT

Patient and partner should be treated

Drugs of choiceCeftriaxoneQuinolone

CHLAMYDIA

Chlamydia trachomatis, gram (-)

IP: 2-10 days


SIGNS AND SYMPTOMS Maybe asymptomatic Gray white discharge, Burning and itchiness

at the urethral opening

DX: Gram stain Antigen detection test on cervical smear Urinalysis


Rex Karl S. Teoxon, R.N, M.D 48

CHLAMYDIADIAGNOSIS

CHLAMYDIAMANIFESTATIONS IN MEN

Urethritis

Proctitis

Epididymitis

CHLAMYDIAMANIFESTATIONS IN WOMEN

UrethritisEndocervicitisProctitisPIDPerihepatitis

MANAGEMENT

Doxycycline or Azithromycin Erythromycin and Ofloxacin

CX: PID Ectopic pregnancy Fetus transmittal (vaginal birth)


SYPHILIS

Figure 26.9a

SYPHILIS Treponema pallidum Invades mucosa or through skin breaks.

Figure 26.10

SYPHILIS Direct diagnosis Darkfield microscopic identification of bacteria Staining with fluorescent-labeled, monoclonal antibodies

Indirect, serological diagnosis VDRL, RPR, ELISA test for reagin-type antibodies using

cardiolipid (Ag) FTA-ABS tests for anti-treponemal antibodies

SYPHILIS

Figure 3.6b

SYPHILIS Primary stage: Chancre at site of infection Secondary: Skin and mucosal rashes Latent period: No symptoms Tertiary: Gummas on many organs Congenital: Neurological damage Primary and secondary stages treated with penicillin

Virulence Factors of T. pallidum

Outer membrane proteins promote adherence Hyaluronidase may facilitate perivascular infiltration Antiphagocytic coating of fibronectin Tissue destruction and lesions are primarily result of

host’s immune response (immunopathology)

SYPHILIS

Treponema pallidum, spirocheteIP: 10-90 days


SYPHILISMECHANISMS OF TRANSMISSION

Sexual contact

Perinatal

SYPHILISFREQUENCY

Incidence has increased , especially in females aged 15-24 years

Highest prevalence - urban blacks and hispanics

SYPHILISCLASSIFICATION

PrimarySecondaryLatent

EarlyLate

Tertiary

SIGNS AND SYMPTOMS Primary (3-6 wks after contact) – nontender

lymphadenopathy and chancre; most infectious; resolves 4-6 wks

Secondary – systemic; generalized macular papular rash including palms and soles and painless wartlike lesions in vulva or scrotum (condylomata lata) and lymphadenopathy

Tertiary – (6-40 years) - neurosyphilis/ permanent damage (insanity); gumma (necrotic granulomatous lesions), aortic aneurysm


Primary disease process involves invasion of mucus membranes, rapid multiplication & wide dissemination through perivascular lymphatics and systemic circulation Occurs prior to development of the primary lesion

10-90 days (usually 3-4 weeks) after initial contact the host mounts an inflammatory response at the site of inoculation resulting in the hallmark syphilitic lesion, called the chancre (usually painless) • Chancre changes from hard to ulcerative with profuse shedding of

spirochetes • Swelling of capillary walls & regional lymph nodes w/ draining• Primary lesion heals spontaneously by fibrotic walling-off within

two months, leading to false sense of relief

Pathogenesis of T. pallidum (cont.)Primary Syphilis

PRIMARY SYPHILISPRINCIPAL CLINICAL FINDING

Secondary disease 2-10 weeks after primary lesion Widely disseminated mucocutaneous rash Secondary lesions of the skin and mucus membranes

are highly contagious Generalized immunological response

Pathogenesis of T. pallidum (cont.)

Secondary Syphilis

SECONDARY SYPHILISPRINCIPAL CLINICAL FINDINGS

Generalized Mucocutaneous

Rash of Secondary Syphilis

SECONDARY SYPHILISPRINCIPAL CLINICAL FINDINGS

LATE STAGE SYPHILISPRINCIPAL CLINICAL MANIFESTATIONS

Destructive gummasAortic valve injuryCNS manifestations

DementiaTabes dorsalisPupillary abnormalities

Following secondary disease, host enters latent period

• First 4 years = early latent

• Subsequent period = late latent

About 40% of late latent patients progress to late tertiary syphilitic disease


Latent Stage Syphilis

Tertiary syphilis characterized by localized granulomatous dermal lesions (gummas) in which few organisms are present • Granulomas reflect containment by the immunologic reaction of

the host to chronic infection Late neurosyphilis develops in about 1/6 untreated cases,

usually more than 5 years after initial infection• Central nervous system and spinal cord involvement • Dementia, seizures, wasting, etc.

Cardiovascular involvement appears 10-40 years after initial infection with resulting myocardial insufficiency and death


Tertiary Syphilis

LATE STAGE SYPHYLISGUMMAS

CONGENITAL SYPHILISCLINICAL MANIFESTATIONS

Fetal deathGrowth restrictionMultiple anomalies

Immediately apparent at birth

Delayed appearance

Congenital syphilis results from transplacental infection

T. pallidum septicemia in the developing fetus and widespread dissemination

Abortion, neonatal mortality, and late mental or physical problems resulting from scars from the active disease and progression of the active disease state


Congenital Syphilis

CONGENITAL SYPHILISRISK OF PERINATAL TRANSMISSION

0

5

10

15

20

25

30

35

40

45

50

Primary Second Early Late/ Tertiary

%

SYPHILISDIAGNOSIS

Clinical examinationDarkfield microscopySerology

VDRL – screening testMHA or FTA – confirmatory test

DIAGNOSIS

Dark-field examination of lesion- 1st and 2nd stage

Non specific VDRL and RPR FTA-ABS

Mgmt Primary and secondary - Pen G Tertiary - IV Pen G


Diagnostic Tests for Syphilis

NOTE: Treponemal antigen tests indicate experience with a treponemal infection, but cross-react with antigens other than T. pallidum ssp. pallidum. Since pinta and yaws are rare in USA, positive treponemal antigen tests are usually indicative of syphilitic infection.

(Original Wasserman Test)

SYPHILISTREATMENT

Patient and sexual partner(s) should be treated

Antibiotic therapyPenicillin – preferred in pregnancy

DoxycyclineTetracycline

Prevention & Treatment of Syphilis

Penicillin remains drug of choice• WHO monitors treatment recommendations• 7-10 days continuously for early stage• At least 21 days continuously beyond the early stage

Prevention with barrier methods (e.g., condoms) Prophylactic treatment of contacts identified through

epidemiological tracing

LYMPHOGRANULOMA VENEREUM (LGV)

Chlamydia trachomatis Initial lesion on genitals heals Bacteria spread through lymph causing

enlargement of lymph nodes

Treatment: Doxycycline

LGVCLINICAL MANIFESTATIONS

CHLAMYDIALGVSTD caused by serovars L1, L2, L3

Common in Asia, Africa, South America, and the Caribbean

Incubation period 3 days to 3 weeks

Painless vesicleregional lymphaticsinguinal and femoral adenitis and proctitis

CHANCROID (SOFT CHANCRE)

Haemophilus ducreyi Ulcer on genitalia May break through surface Infection of lymph nodes Treatment: Erythromycin and ceftriaxone

BACTERIAL VAGINOSIS Gardnerella vaginalis

Diagnosis by clue cells

Treatment: Metronidazole

Figure 26.12

DIAGNOSIS

Viral culture Pap smear (shows cellular changes) Tzanck smear (scraping of ulcer for staining)


MANAGEMENT

Anti viral – acyclovir (zovirax)CX: Meningitis – mild and self limiting Neonatal infection (vaginal birth)

Disseminated with liver involvement Encephalitis Skin, eyes, mouth


GENITAL HERPES

Herpes simplex virus 2 (Human herpesvirus 2 or HHV–2)

Neonatal herpes transmitted to fetus or newborns

Recurrences from viruses latent in nerves Suppression: Acyclovir or valacyclovir

HERPES GENITALIS

HSV 2 Envelop, icosahedral, dsDNA Latent – sacral nerve ganglia


SIGNS AND SYMPTOMS

Painful sexual intercourse Painful vesicular lesions (cervix, vagina,

perineum, glans penis)


GENITAL WARTS Human papillomaviruses Treatment: Imiquimod to stimulate interferon HPV 16 causes cervical cancer and cancer of the

penis. DNA test is needed to detect cancer-causing strains. Vaccination against HPV strains

GENITAL WARTS

Condyloma Acuminatum HPV type 6 & 11, papilloma virus


SIGNS AND SYMPTOMS Single or multiple soft, fleshy painless

growth of the vulva, vagina, cervix, urethra, or anal area, Vaginal bleeding, discharge, odor and dyspareunia

DX: Pap smear-shows cellular changes

(koilocytosis) Acetic acid swabbing (will whiten lesion)



MANAGEMENT

Laser treatment is more effective

CX: Neoplasia Neonatal laryngeal papillomatosis

(vaginal birth)

CANDIDIASIS Candida albicans Grows on mucosa of mouth, intestinal tract, and

genitourinary tract. NGU in males Vulvovaginal candidiasis Diagnosis is by microscopic identification and culture

of yeast. Treatment: Clotrimazole or miconazole.

CANDIDIASIS

Moniliasis (oral candidiasis) Vulvovaginal candidiasis Candida albicans (Yeast or fungus)


SIGNS AND SYMPTOMS

Cheesy white discharge Extreme itchiness

DX: KOH (wet smear indicate positive result)


MANAGEMENT

Imidazole, Monistat, Diflucan

CX: Oral thrush to baby (vaginal birth)


TRICHOMONIASIS Trichomonas vaginalis Found in semen or urine of

male carriers Vaginal infection causes

irritation and profuse discharge.

Diagnosis is by microscopic identification of protozoan.

Treatment: Metronidazole.

Figure 26.15

TRICHOMONIASIS

Trichomonas vaginalis parasite


SIGNS AND SYMPTOMS

Females: itching, burning on urination, yellow gray frothy malodorous vaginal discharge, foul smelling

Males: usually asymptomatic

Dx: microscopic exam of vaginal discharge


MANAGEMENT

Metronidazole (Flagyl) include partners

CX: PROM


VAGINITIS AND VAGINOSIS

Table UN 26.1

KNOW NORMAL!

1. Epithelial Cells

2. Lactobacilli- 5 to 15 µ

3. WBCs- Few = NL- Never > Epi’s- Many = Inflammation

(Parabasilar Cell) >

VAGINOSIS - KNOW 3

1. Bacterial Vaginosis- FEW or NO LACTOBACILLI

- MANY Coccobacillary Orgs.

= “GARBAGE”

- CLUE CELLS

= CELL EDGE

- FEW WBCs!!!!!!!

- MOBILUNCUS = MOTILE

2. Cytolytic Vaginosis= “LactobacillusOvergrowth Syndrome”- MANY LACTOBACILLI

- 5 to 15 µ

VAGINOSIS - KNOW 3

3. Lactobacillosis/Leptothrix- LONG LACTOBACILLI- 40 to 75 µ

VAGINITIS - KNOW 2+

1. Trichomonas

2. Candidiasis/Yeast- Candida albicans 1) Blastospores “CANDIDIASIS” 2) Budding Yeast

3) Pseudohyphae

- Candida glabrata 1) Blastospores (Torulopsis g.) 2) Budding yeast “YEAST”

Grow is clusters = CUMULI >

ADDITIONAL SLIDES - NORMALS

Normal Epithelial Cells with Sharp Borders

Normal Lactobacilli - 5 to 15 µ (note size relative to cell nucleus)

ADDITIONAL SLIDES - CLUE CELLSAND INFLAMMATION OF ? CAUSE

STD



HIV AND AIDS

Retrovirus (HIV1 & HIV2)Attacks and kills CD4+

lymphocytes (T-helper)Capable of replicating in the

lymphocytes undetected by the immune system

Immunity declines and opportunistic microbes set in

No known cure

MOT

Sexual intercourse (oral, vaginal and anal) Exposure to contaminated blood, semen, breast

milk and other body fluids Blood Transfusion IV drug use Transplacental Needle stick injuries



HIGH RISK GROUP

Homosexual or bisexual Intravenous drug users BT recipients before 1985 Sexual contact with HIV+ Babies of mothers who are HIV+

SIGNS AND SYMPTOMS

1. Acute viral illness (1 mo after initial exposure) – fever, malaise, lymphadenopathy

2. Clinical latency – 8 yrs w/ no sx; towards end, bacterial and skin infections and constitutonal sx – AIDS related complex; CD4 counts 400-200

3. AIDS – 2 yrs; CD4 T lymphocyte < 200 w/ (+) ELISA or Western Blot and opportunistic infections


DIAGNOSIS

HIV+ 2 consecutive positive ELISA and 1 positive Western Blot TestAIDS+ HIV+ CD4+ count below 200/ml



SIGNS AND SYMPTOMS

Extreme fatigue Intermittent fever Night sweats Chills Lymphadenopathy Enlarged spleen

SIGNS AND SYMPTOMS Anorexia Weight loss Severe diarrhea Apathy and depression PTB Kaposis sarcoma Pneumocystis carinii AIDS dementia


MANAGEMENT

Nucleoside Reverse Transcriptase Inhibitors NRTI’sZidovudine (AZT) – limit viral growth

Non-nucleoside Reverse Transcriptase Inhibitors NNRTI’s Ritonavir (Norvir)

Prevention of spread (safe sex)Universal precautionsSymptomatic intervention and

treatment of opportunistic infectionsVaccines (influenza and hepa B) 139Rex Karl S. Teoxon, R.N, M.D

utigutimicro

Health & Medicine

urinary system

female urinary organsfigure

reproductive systemsmicrobes

inflammation of urethra

coliformsml of urine

inflammation of bladder

ureteritisflank pain

urethritisinguinal pain