CHAPTER 3 PART 3

what are the clinical manifestations of STIs (Skin Lesions)

1. Chancre

2. Chancroid

3. Genital Herpes

4. Granulomatous Reactions

5. Rashes

6. Warty Lesions

• primary lesion of syphilis

• painless

• well-delineated

CHANCRE

• ulcer with ragged edges

• painful

CHANCROID

• start as a vehicle that becomes an ulcer after rapture

GENITAL HERPES

• granuloma inguinale

GRANULOMATOUS REACTIONS

• secondary syphilis

• Gonorrhea

• Candidiasis

RASHES

• Condyloma acuminatum

• Molluscum contagiosum

WARTY LESIONS

Clinical Manifestations of STIs (DISCHARGE)

Vaginal Discharge

• Dysuria

• Dyspareunia

• Vulvar Irritation

it is thin, foamy, and foul-smelling vaginal discharge

Trichomonas vaginalis

a greenish and purulent vaginal discharge

Neisseria gonorrhea

a thick, cheesy exudates (milk curd-like appearance) vaginal discharge

Candida albicans

• Spirochete with fine regular coils with tapered ends

• Strictly a human pathogen

• Sensitive to oxygen

• Cannot grow in cell-free culture medium

Treponema pallidum

clinical findings for Treponema pallidum

1. Adult Syphilis

2. Congenital Syphilis

   • Early Congenital Syphilis (right after birth)

   • Late Congenital Syphilis

Adult Syphilis

• right after birth

• May be asymptomatic

• Runny nose (snuffles), rash, condylomata, and hepatosplenomegaly

Early Congenital Syphilis

• Manifested at 8th nerve deafness with bone and teeth deformities

  • saddle nose

  • saber shins

  • Hutchinson’s teeth, and

  • Mulberry or Moon’s molars

Late Congenital Syphilis

laboratory diagnosis for Treponema pallidum

• Darkfield microscopy

• Serology

  • Non-specific treponemal test – VDRL (Venereal Disease Research Laboratory) and RPR (Rapid Plasma Reagin)

  • Specific treponemal test – Fluorescent Treponemal Antibody Absorption (FTA-ABS)

treatment and prevention for Treponema pallidum

• DOC: Penicillin

• Alt.: Tetracycline and Doxycycline

• “Gonococci”

• Gram (-) diplococcus;

• kidney bean-shaped (single) and coffee bean-shaped (pairs)

• Virulence Factor: Pili

Neisseria gonorrhoeae

mode of transmission for Neisseria gonorrhoeae

Sexual contact

Gonorrhea in males

• painful urination

• a discharge of pus-containing material

• 80% —> after incubation period

• most patients —> < a week

Gonorrhea in females

• cervix (columnar epithelial cells)

• most are asymptomatic

• Complication —> Pelvic Inflammatory Disease (IPD)

Disseminated Gonorrhea

• (1% - 3%) fever, migratory arthralgia, suppurative arthritis of the wrists, knees, and ankles, and pustules with erythematous base over the extremities

• Other diseases associated:

  • Perhepatitis (Fitz-Hugh-Curtis Syndrome)

  • Purulent conjunctivitis (adults)

  • Infected mother —> infant (Ophthalmia Neonaturum) —> Blindness

laboratory diagnosis for Neisseria gonorrhoeae

Culture (Thayer-Martin Medium)

treatment and prevention for Neisseria gonorrhoeae

• Uncomplicated – Ceftriaxone, Ciprofloxacin, Cefixime, or Ofloxacin

• Mixed Infection with Chlamydia – uncomplicated med + Doxycycline or Azithromycin

• Ophthalmia neonatorum – Prevention: 1% AgNO3 or 5% Erythromycin or Tetracycline ointment

• Obligate intracellular bacteria

• Process of development (2 forms)

  • Elementary bodies – metabolically inactive infectious

  • Reticulate bodies – metabolically-active noninfectious

• Serotypes D-K: non-gonococcal urethritis (NGU), cervicitis, and PID

• Serotypes L1, L2, and L3: lymphogranuloma venereum

Chlamydia trachomatis

clinical findings for Chlamydia trachomatis

• Urogenital Tract Infections

• Lymphogranuloma Venereum (LGV)

• Most are asymptomatic

• Symptomatic:

  • cervicitis

  • endometritis

  • urethritis

  • salpingitis

  • bartholinitis

  • perihepatitis, and

  • mucopurulent discharge

Urogenital Tract Infections

• Primary stage: a lesion appears at the site of infection, either a papule or ulcer, which is small, painless, and heals rapidly

• Secondary stage: enlarged lymph nodes that are painful (buboes) and ruptures to form draining fistulas

Lymphogranuloma Venereum (LGV)

Laboratory Diagnosis for Chlamydia trachomatis

Giemsa staining (using scrapings from the lesion —> inclusion bodies)

treatment and prevention for Chlamydia trachomatis

• Azithromycin

• Doxycycline or

• Erythromycin

• Gram (-) coccobacillus

• Only requires hemin (X factor) for growth (from blood)

• Virulence Factor: Pili

Haemophilus ducreyi

clinical findings for Haemophilus ducreyi

Chancroid

A soft, painful papule with an erythematous base that develops into an ulcer with ragged edges associated with inguinal lymphadenopathy

Chancroid

Laboratory Diagnosis for Haemophilus ducreyi

Culture (in at least kinds of enriched media with VANCOMYCIN)

treatment and prevention for Haemophilus ducreyi

• Cephalosporins

• Azithromycin

• Erythromycin or

• Ciprofloxacin

what are the symptoms of Urinary Tract Infection (UTI)

• Community-acquired UTI

• Nosocomial UTI

symptoms of UTI where:

• More common in women —>(shorter urethra and proximity of anal opening to the urethral orifice)

• Mostly uncomplicated

Community-acquired UTI

symptoms of UTI where:

• Complications of prolonged urethral catheterization (most are resistant to various antibiotics)

Nosocomial UTI

What are the predisposing factors of UTI?

1. Gender - UTI is more common in females especially school-aged girls and those above 60 years of age.

2. Mechanical factors - catheterization, sexual intercourse, kidney stones, and improper use of tampons and douches.

3. Metabolic disorders - increased sugar content of urine, due to diabetes, for instance, is conducive to bacterial growth.

4. Anatomic abnormalities of the urinary tract - can lead to obstruction or incomplete voiding of urine or reflux of urine.

causative agents of UTI

• Escherichia coli

• Proteus mirabilis

• Serratia spp.

• Enterococcus faecalis

• Staphylococcus saprophyticus

it is the causative agent of UTI where:

• G (-) bacillus

• Part of the normal flora (colon)

• The most common cause of community-acquired UTIs

• Improper washing after defecation

Escherichia coli

causative agent of UTI where:

• G (-) bacillus

• Urease (+) –> alkalinization of the urine

• Major cause of nosocomial UTIs

• 2nd most common cause of community-acquired UTIs

Proteus mirabilis

causative agent of UTI where:

• Serratia marcescens

• Prodigosin (imparts red color)

• G (-) bacillus

• Infections are associated with underlying disease, changing physiological patterns, immunosuppressive therapy, mechanical manipulation of patients

Serratia spp.

the causative agent of UTI where:

• G (+) coccus

• Part of the enteric flora

• Grows in 6.5% NaCl

• Causes nosocomial UTIs

Enterococcus faecalis

causative agent of UTI where:

• G (+) coccus

• Common cause of UTI in sexually active young women

Staphylococcus saprophyticus

clinical findings for UTI

1. Cystitis

2. Urethritis

3. Pyelonephritis

4. Urethrocystitis

• inflammation of the urinary bladder

  • suprapubic pain and tenderness, frequency of urination, and occasional hematuria

Cystitis

• inflammation of the urethra

  • dysuria, frequency, and urgency of urination

Urethritis

• inflammation of the kidneys

  • flank pain, fever, chills, hematuria, kidney punch

Pyelonephritis

malodorous urine, especially in women, incontinence

Urethrocystitis

laboratory diagnosis for UTI

• Urinalysis

• Urine Culture

treatment and prevention for UTI

• Uncomplicated Infection (E. coli) – Co-trimoxazole

• Proteus and Pseudomonas – DOC: Fluoroquinolones

• Acute Pyelonephritis – Fluoroquinolones or 3rd Generation cephalosporins

• Susceptibility testing

• All transmitted by the bite of arthropods except Q fever (inhalation)

• All are zoonotic except Endemic Typhus (which occurs only in humans)

• Groups:

  • Typhus Group – Epidemic, Murine (Endemic), Scrub

  • Spotted Fever Group – Rocky Mountain Spotted Fever

  • Traditional Group – Rickettsialpox

  • Q Fever

  • Trench Fever

  • Ehrlichiosis

Rickettsial Infections

• Gram (-) pleomorphic

• Obligate intracellular parasite

• Stain well using Giemsa or Gimenez Stain

• Growth enhanced by sulfonamides

Rickettsial Infections

Diseases under Rickettsial Infections

1. Rocky Mountain Spotted Fever

2. Rickettsialpox

3. Epidemic Typhus

4. Murine Typhus

5. Scrub Typhus

6. Q (Query) Fever

7. Ehrlichiosis

   • Human monocyte ehrlichiosis

   • Human granulocyte ehrlichiosis

   • Erwingii ehrlichiosis

   • Sennetsu Fever

• Etiology: Rickettsia rickettsii

• Vector: Tick

• Reservoir: Ticks, Wild rodents

• Manifestations: Maculopapular rashes appear on the hands and feet —> later in the trunk (2-6 days)

Rocky Mountain Spotted Fever

• Etiology: Rickettsia akari

• Vector: Mite

• Reservoir: Mites, Wild rodents

• Manifestations:

  • A mild disease resembling varicella

  • Fever, headache, chills, myalgia, the appearance of a firm red macule at the bite site —> deep-seated vesicle that ruptures —> ESCHAR

Rickettsialpox

• Etiology: Rickettsia prowazekii

• Vector: Louse

• Reservoir: Humans (primary reservoir), squirrel fleas, flying squirrels

• Manifestations:

  • Maculopapular rashes (sparing palms and soles)

  • More severe systemic infection; more fatal

  • Associated with Brill-Zinsser Disease

Epidemic Typhus

• Etiology: Rickettsia typhi

• Vector: Flea

• Reservoir: Wild rodents

• Manifestations: Similar to Epidemic typhus but milder and rarely fatal except in the elderly

Murine Typhus

• Etiology: Orientia/Rickettsia tsutsugamushi

• Vector: Mite

• Reservoir: Mites, Wild rodents

• Manifestations:

  • Resembles Epidemic Typhus except for the Eschar

  • Generalized lymphadenopathy and lymphocytosis

  • May also involve severe cardiac and cerebral complications

Scrub Typhus

• Etiology: Coxiella burnetti

• Vector: None ( via inhalation of spores)

• Reservoir: Cattle, Sheep, Goats, Cats

• Manifestations:

  • Resembles influenza and non-bacterial pneumonia, hepatitis or encephalopathy

  • Does not present any rash or local lesion

Q (Query) Fever

• Etiology:

• Vector: Tick

• Reservoir: Ticks

• Manifestations:

  • Parasitize lymphocytes, neutrophils, and monocytes

  • Manifest non-specific symptoms with thrombocytopenia

Ehrlichiosis

Etiology of Human monocyte ehrlichiosis

Ehrlichia chaffeensis

Etiology of Human granulocyte ehrlichiosis

Anaplasma phagocytophilum

Etiology of Erwingii ehrlichiosis

Ehrlichia ewingii

Etiology of Sennetsu Fever

Ehrlichia sennetsu

• Spirochete

• Reservoir Host: Rats

  • excreted in the urine and contaminated soil and water

Leptospira interrogans

mode of transmission for Leptospira interrogans

• The organism enters through breaks in the skin or mucous membranes

• Ingestion of contaminated food and water

clinical findings of Leptospira interrogans

Leptospirosis

• 1st Stage: flu-like symptoms —> fever, severe headache, myalgia, and chills

• 2nd Stage: (immune period) —→ s/sx of meningitis

• Severe cases: impaired renal function and liver damage (Weil’s Disease/Infective Jaundice)

laboratory diagnosis for Leptospira interrogans

• Darkfield Microscopy

• Increase in agglutinating antibodies

treatment and prevention for Leptospira interrogans

• Recommended drug – Penicillin

• Prophylaxis – Doxycycline

• Preventive Measures:

  • Avoid wading in contaminated water

  • Avoid contact with contaminated soil

  • Rodent control

• Spirochete with coarse, irregular coils

• Reservoir: Wood Rat

• Host: Mammals (Deer – where the tick completes its life cycle)

Borrelia burgdorferi

mode of transmission for Borrelia burgdorferi

Bite of a tick (Ixodes)

clinical findings for Borrelia burgdorferi

Lyme Disease (Lyme Borreliosis)

• 1st Stage: painless, circular red rash (erythema chronicum migrans) with a clear center at the site of the bite, athralgia, fever, headache, chills, and fatigue (with or without)

• 2nd Stage(after a few weeks/months): myocarditis/pericarditis, aseptic meningitis, Bell’s palsy, and neuropathies

• Latent Period (several weeks or months)

• 3rd Stage: arthritis (large joints) and progressive chronic involvement of the CNS

laboratory diagnosis for Borrelia burgdorferi

• Giemsa or Silver stains

• Darkfield Microscopy

• Serological tests (ELISA or Indirect immunofluorescence)

• Confirmatory Test – Western Blot Assay or PCR (Polymerase Chain Reaction)

Treatment and Prevention for Borrelia burgdorferi

• Mild Infections – Amoxicillin or Doxycycline

• Late Stage – Pen G or Ceftriaxone

• Spirochete; highly flexible and highly motile (rotatory and twitching)

• Can survive at low temperature (4 degrees C) in blood or culture

• Reservoir: Rodents

Borrelia recurrentis

mode of transmission for Borrelia recurrentis

• Bite of a human body louse (Pediculus humanus) – Louse-borne relapsing fever

• Bite of ticks (Ornithodorus) – Tick-borne relapsing fever

clinical findings for Borrelia recurrentis

Relapsing Fever

• Fever, headache, and chills

• The fever lasts for a few days and resolves but recurs after a week with associated multi-organ dysfunction.

• 3-10 recurrences (with each recurrence manifestations become less severe)

laboratory diagnosis for Borrelia recurrentis

Giemsa or Wright Stain (the best time for sample collection is during the height of the fever)

Infections of the eyes

• Conjunctivitis

• Keratitis

• Keratoconjunctivitis

• Pink eye conjunctivitis

• Highly contagious

• Manifestations: eye irritation, reddening of the conjunctiva, swelling of the eyelids, mucopurulent discharge, and photophobia

Bacterial Conjunctivitis

Etiologic Agents of Bacterial Conjunctivitis

• Haemophilus influenzae

• Streptococcus pneumoniae

• Staphylococcus aureus

• Pseudomonas aeruginosa

• Chlamydia trachomatis

• Neisseria gonorrhoeae

• Koch-Weeks bacillus

• G(-) coccobacillus

• Virulence Factor: Pili

• Epidemics of acute, purulent conjunctivitis (summer months)

• Transmission: Gnat Fly (mechanical vector)

Haemophilus influenzae biogroup aegyptius

• most common cause of NGU

• “swimming pool conjunctivitis”

• inclusion conjunctivitis – newborn babies

• Trachoma - chronic keratoconjunctivitis caused by serotypes A, B, Ba, and C

  • Symptoms: Eye pain, Swelling eyelids, and Eye irritation

• Transmission:

  • eye-to-eye by droplets, fomites, flies, feces, and respiratory droplets

Chlamydia trachomatis

Ophthalmia Neonatorum

Neisseria gonorrhoea

Infections of the Nervous System

• Encephalitis (brain parenchyma)

• Encephalomyelitis (brain and spinal cord)

• Meningitis (pia and arachnoid matter)

  • Meningism - symptoms that signifies the occurrence of meningitis

• Meningoencephalitis (brain and meninges)

• Myelitis (spinal cord)

• TRIADS - fever, headache, and nuchal rigidity (stiff neck)

• ETIOLOGIC AGENTS:

  • Escherichia coli - the most common cause of this disease in newborn

  • Haemophilus influenzae Type B (Hib) - Hib-caused meningitis occurs mostly in children under age 4, especially at about 6 months when antibody protection provided by the mother weakens.

  • Neisseria meningitidis (Meningococcus)

  • Listeria monocytogenes

Acute Bacterial Meningitis

• G(-)

• coffee-bean/kidney-shaped diplococcus

• Transient flora of the nasopharynx (carriers)

• Virulent Factor: Endotoxin

Neisseria meningitidis

mode of transmission for Neisseria meningitidis

• Respiratory droplets (main mode)

• Carriers

clinical findings for Neisseria meningitidis

Meningococcal Meningitis (Meningococcemia)

• Under 2 years of age (residual damage – deafness)

• Throat infection → bacteremia → meningitis

• Rash: petechiae or purpuric skin lesions over the trunk and in lower extremities (does not fade when pressed)

• Complication: Waterhouse-Friderichsen syndrome (destruction of the adrenal gland)

laboratory diagnosis for Neisseria meningitidis

• Culture of the organism (Blood and CSF)

• Gram-staining

• Detection of polysaccharide antigen

treatment and prevention for Neisseria meningitidis

• Penicillin -DOC

• Chloramphenicol and 3rd gen cephalosporins - alternative

• Minocycline and rifampicin - treatment of carriers

• Sulfonamides and rifampicin - prophylaxis

• Cold-loving (capable of growth at 1 degree C) but are also capable of growth at 45 degrees C and in high salt concentration

• Tumbling motility

• Mainly infects immunocompromised patients

Listeria monocytogenes

mode of transmission for Listeria monocytogenes

• Ingestion of contaminated food products (primary source)

• Transplacental transmission (during pregnancy/birth)

clinical findings for Listeria monocytogenes

Newborns

• Early-onset Listeriosis – acquired during pregnancy

  • Granulomatous infantiseptica – severe form

• Late-onset Listeriosis – acquired during or right after delivery

  • Meningitis or meningitis + encephalitis with septicemia

laboratory diagnosis for Listeria monocytogenes

• Culture (blood, spinal fluid, or the placenta)

  • Cold enrichment media

• Observation of tumbling end-to-end motility

treatment and prevention for Listeria monocytogenes

TOC: Penicillin or ampicillin either singly or combined with gentamicin

clinical findings for Mycobacterium tuberculosis

Tuberculosis Meningitis

• Affects children younger than 6 years old

• Usually appears 3-6 months after the initial infection

• Accompanies Military Tuberculosis (50% cases)