Microbial Diseases of the Urinary and Reproductive Systems

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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 y S. saprophyticus y May also be caused by Proteus Klebsiella Enterococcus Pseudomonas E. coli usually causes pyelonephritis. Antibiotic-sensitivity tests may be required before treatment.
y

UTI
Ureteritis = 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)

³BAD STROKE´

FACTORS THAT CONTRIBUTE TO UTI
(PROXIMITY TO THE ANUS, SHORTER URETHRA) POOR HYGIENE UNSAFE SEXUAL PRACTICES BACK TO FRONT STROKE HIGH pH URINARY STASIS KIDNEY STONES OBSTRUCTION OF URINE OUTFLOW
FEMALE

S/Sx: PAIN assessment Pain during and after urination = cystitis Pain after urination = urethritis Inguinal pain = ureteritis Flank pain = pyelonephritis Inflammatory manifestations fever and chills Cx: Ascending infection Obstruction (stones/calculi)

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 urinecontaminated 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 interrogans) species epithet ±

Leptospirosis Clinical Syndromes 
Mild virus-like syndrome  (Anicteric leptospirosis) Systemic with aseptic meningitis  (Icteric leptospirosis) Overwhelming disease (Weil¶s disease) 
Vascular collapse Thrombocytopenia Hemorrhage Hepatic and renal dysfunction NOTE: Icteric refers to jaundice (yellowing of skin and mucus membranes by deposition of bile) and liver involvement

Pathogenesis of Icteric Leptospirosis 
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 lesion ii. Infects the kidneys and organisms are shed in the urine (leptospiruria) with renal failure and death not uncommon 

Hepatic injury & meningeal irritation is common

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
y y y y

Endocarditis Meningitis Arthritis Ophthalmia neonatorum

GONORRHEA

Figure 26.7

GONORRHEA

UN 26.1

NONGONOCOCCAL URETHRITIS

Chlamydia trachomatis
y y

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

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SIGNS AND SYMPTOMS

Females: usually asymptomatic or minimal urethral discharge w/ lower abdominal pain Male: Mucopurulent discharge, Painful urination

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GONORRHEA MANIFESTATIONS IN MEN 

Urethritis Epididymitis Proctitis Pharyngitis

GONORRHEA CLINICAL PRESENTATION

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GONORRHEA MANIFESTATIONS IN WOMEN 

Urethritis Endocervicitis Proctitis PID Pharyngitis

GONORRHEA DISSEMINATED INFECTION 
Arthritis Dermatitis Pericarditis Meningitis Perihepatitis

and endocarditis

DISSEMINATED GONORRHEA CLINICAL PRESENTATION

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DIAGNOSIS

GSCS of cervical secretions on Thayer Martin medium

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GONORRHEA GRAM STAIN

GONORRHEA DIAGNOSIS 

Clinical

examination Gram stain Culture Nucleic acid probes

MANAGEMENT
Ceftriaxone (Rocephin) 250 mg IM Ofloxacin (Floxin) 400 mg orally treat concurrently with Doxycycline or Azithromycin for 50% infected w/ Chlamydia

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GONORRHEA SEQUELAE 

Infertility Ectopic

pregnancy Chronic pelvic pain

COMPLICATION
PID ectopic pregnancy and infertility Peritonitis Perihepatitis Ophthalmia neonatorum Sepsis Arthritis

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GONORRHEA TREATMENT
Patient

and partner should be treated Drugs of choice
y Ceftriaxone y Quinolone

CHLAMYDIA

Chlamydia trachomatis, gram (-)

IP: 2-10 days

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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

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CHLAMYDIA DIAGNOSIS

CHLAMYDIA MANIFESTATIONS IN MEN 

Urethritis Proctitis Epididymitis

CHLAMYDIA MANIFESTATIONS IN WOMEN 
Urethritis Endocervicitis Proctitis PID Perihepatitis

MANAGEMENT
Doxycycline or Azithromycin Erythromycin and Ofloxacin

CX: PID Ectopic pregnancy Fetus transmittal (vaginal birth)

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SYPHILIS

Figure 26.9a

SYPHILIS pallidum Treponema

Invades mucosa or through skin breaks.

Figure 26.10

SYPHILIS Direct diagnosis
y y

Darkfield microscopic identification of bacteria Staining with fluorescent-labeled, monoclonal antibodies VDRL, RPR, ELISA test for reagin-type antibodies using cardiolipid (Ag) FTA-ABS tests for anti-treponemal antibodies

Indirect, serological diagnosis
y y

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, spirochete IP: 10-90 days

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SYPHILIS MECHANISMS OF TRANSMISSION 

Sexual

contact 

Perinatal

SYPHILIS FREQUENCY 

Incidence

has increased , especially in females aged 15-24 years Highest prevalence - urban blacks and hispanics

SYPHILIS CLASSIFICATION 
Primary Secondary Latent 

Early Late 
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

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Pathogenesis of T. pallidum (cont.) Primary Syphilis 
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

PRIMARY SYPHILIS PRINCIPAL CLINICAL FINDING

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Pathogenesis of T. pallidum (cont.) Secondary Syphilis 
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

SECONDARY SYPHILIS PRINCIPAL CLINICAL FINDINGS

Generalized Mucocutaneous Rash of Secondary Syphilis

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SECONDARY SYPHILIS PRINCIPAL CLINICAL FINDINGS

LATE STAGE SYPHILIS PRINCIPAL CLINICAL MANIFESTATIONS
Destructive

gummas Aortic valve injury CNS manifestations
y Dementia y Tabes

dorsalis y Pupillary abnormalities

Pathogenesis of T. pallidum (cont.) Latent Stage Syphilis 
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

Pathogenesis of T. pallidum (cont.) Tertiary 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

LATE STAGE SYPHYLIS GUMMAS

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CONGENITAL SYPHILIS CLINICAL MANIFESTATIONS

Fetal

death Growth restriction Multiple anomalies
y Immediately

apparent at birth y Delayed appearance

Pathogenesis of T. pallidum (cont.) Congenital Syphilis 
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 RISK OF PERINATAL TRANSMISSION
50 45 40 35 30

% 20
15 10 5 0 Primary Second Early Late/Tertiary

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SYPHILIS DIAGNOSIS

Clinical

examination Darkfield microscopy Serology
y VDRL ±

screening test y MHA 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

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Diagnostic Tests for Syphilis

(Original Wasserman Test)

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.

SYPHILIS TREATMENT
Patient

and sexual partner(s) should be treated Antibiotic therapy
y Penicillin

± preferred in pregnancy y Doxycycline y Tetracycline

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

LGV CLINICAL MANIFESTATIONS

CHLAMYDIA LGV
STD

caused by serovars L1, L2,

L3 Common in Asia, Africa, South America, and the Caribbean Incubation period 3 days to 3 weeks Painless vesicle regional lymphatics inguinal 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)

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

Disseminated with liver involvement Encephalitis Skin, eyes, mouth

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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

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SIGNS AND SYMPTOMS
Painful sexual intercourse Painful vesicular lesions (cervix, vagina, perineum, glans penis)

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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

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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)

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MANAGEMENT
Laser

treatment is more effective

CX: Neoplasia Neonatal laryngeal papillomatosis (vaginal birth)

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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)

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SIGNS AND SYMPTOMS
Cheesy white discharge Extreme itchiness

DX: KOH (wet smear indicate positive result)

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MANAGEMENT

Imidazole, Monistat, Diflucan

CX: Oral thrush to baby (vaginal birth)

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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

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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

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MANAGEMENT
Metronidazole (Flagyl) include partners

CX: PROM

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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. = ³GARBAGE´ - CLUE CELLS = CELL EDGE - FEW WBCs!!!!!!! - MOBILUNCUS = MOTILE

2.

Cytolytic Vaginosis
= ³Lactobacillus Overgrowth 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
³CANDIDIASIS´

1) Blastospores 2) Budding Yeast 3) Pseudohyphae 1) Blastospores 2) Budding yeast

- Candida glabrata (Torulopsis g.)
³YEAST´

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 CELLS AND INFLAMMATION OF ? CAUSE

STD

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HIV AND AIDS
Retrovirus

(HIV1 & HIV2) Attacks and kills CD4+ lymphocytes (Thelper) Capable of replicating in the lymphocytes undetected by the immune system Immunity declines and opportunistic microbes set in No known cure
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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

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

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SIGNS AND SYMPTOMS
1.

2.

3.

Acute viral illness (1 mo after initial exposure) ± fever, malaise, lymphadenopathy Clinical latency ± 8 yrs w/ no sx; towards end, bacterial and skin infections and constitutonal sx ± AIDS related complex; CD4 counts 400-200 AIDS ± 2 yrs; CD4 T lymphocyte < 200 w/ (+) ELISA or Western Blot and opportunistic infections

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

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SIGNS AND SYMPTOMS
Extreme fatigue Intermittent fever Night sweats Chills Lymphadenopathy Enlarged spleen

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

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MANAGEMENT

Nucleoside

Reverse Transcriptase Inhibitors

NRTI¶s Zidovudine (AZT) ± limit viral growth Non-nucleoside Reverse Transcriptase Inhibitors NNRTI¶s Ritonavir (Norvir) Prevention of spread (safe sex) Universal precautions Symptomatic intervention and treatment of opportunistic infections Vaccines (influenza and hepa B)
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