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Infections in the mother and neonate

Increased risk of infection in the newborn due to:

Primary (inherent)
  • Immature host defenses
  • Naïve, inexperienced immune system
  • Poor skin integrity
Secondary (environmental)
  • Hospital environment – exposure to drug-resistant pathogens
  • Medical intervention – invades protective skin and mucous membranes

Protection from transmission

  • Fetal membranes protect from external organisms
  • Placenta protects from maternal organisms
  • Maternal endowment of maternal antibodies into the fetal bloodstream; mostly IgG
  • Breast milk contains IgA, WBC, lysozome

Routes of transmission

  • Maternal infections transmitted to fetus (syphilis, HSV, CMV, HIV, VZV, Rubella, Toxoplasma gondii)
    • Transplacental/Congenital – infections in utero, incidence and effects depend on gestation
    • Prenatal – before birth, present at the time of birth
      • Ascending (via vagina and cervix)
      • Amniotic leakage (rare)
      • Maternal blood (cross placenta into fetal circulation; infection dependant on organisms, placental integrity and trimester)
  • Birth canal/environmental infections transmitted to fetus
    • Perinatal (intrapartum)– just before, during or after birth; haematogenous or via birth canal (CMV, VZV, HIV, HBV, HSV, Chlamydia, Gonorrhoea, GBS)
    • Neonatal – manifest first 4 weeks after birth; infection from environment of breast milk (Hep B, HIV, CMV)

Timing – later is usually better

  • Toxoplasmosis, CMV, rubella – first trimester
  • Syphilis breaches placenta, but only infects in the 5th month
  • Varicella –teratogenic in 1st to early 2nd trimester (rare). More commonly, neonates are infected within 5 days of delivery leading to overwhelming infection

Outcomes –

  • Nonspecific effects following maternal infection – fetal death and preterm delivery
  • Fetal infection (maternal infection often mild, nonspecific or asymptomatic)
    • Transient asyptomatic infection (specific IgM detectable when born )
    • Chronic infection – developmental abnormality, organ damage, growth retardation
      • Interference with organogenesis, particularly eye and cardiac system in first half of pregnancy
      • Inflammatory response to tissue infection, especially in CMV
      • Placental insufficiency, due to placental infection – compromises development, LBW, premature

Prevention of congenital infection

  • Routine antenatal maternal screening for immunity (mainly rubella) and asymptomatic infection (GPS, HBV, syphilis)
  • Intervention to treat maternal infection, prevent/reduce fetal transmission. Chronic maternal infection:
    • Syphilis, GBS – antibiotics
    • HBV (hepB) – perinatal immunization, no breastfeeding, immunoglobulins
    • HIV – antiretroviral therapy, C section, no breast feeding
    • Asymptomatic bacteriuria – antibiotics
    • GBS carriage – intrapartum antibiotics: late (35 weeks pregnancy, penicillin decreases infection by 60%)

Rubella – maternal infection is transient and mild, but fetal damage can be very severe, depending on time:

  • Wk 0-8 – 90-100% chance of multiple defects (CNS/eye/cardiac)
  • Wk 8-12 – 80-90% chance of multiple defects
  • Wk 12-18 – declines to 0% chance of deafness and mental retardation
  • Wk >18 weeks – deafness, rarely

Cytomegalovirus – the most common viral cause of congenital malformation in Australia

  • Transmission – exposure to maternal blood in utero, cervix, breast milk. Later in life – close contact and sexual
  • Hepatosplenomegaly, jaundice, microcephaly, prematurity, chorioretinitis (blindness), mental retardation, hearing loss, petechiae (small purple spots)

Group B streptococcus – normal vaginal flora in 25% of women; commonest cause of neonatal sepsis (whole body inflammation due to infection). Prophylaxis against GBS sepsis: routine antenatal screening (lower vaginal swab) and clinical screening for risk factors; antibiotics.

HIV – (human immunodeficiency virus (retrovirus)) major measures that may reduce vertical transmission

  • Antiretroviral Therapy (ART) – mother antenatal and intrapartum, infant for first 6 weeks of life
  • Elective caesarean section, avoidance of invasive obstetric procedures, limit duration of rupture of the membranes
  • Alternatives to breast feeding
  • Treat other STDs

Varicella Zoster virus – vesicular rashes and scarring; complication include bacterial superinfection of skin lesions, thrombocytopenia, arthritis, hepatitis, meningitis, encephalitis, cerebellar ataxia

Sexually transmitted diseases

Genital warts (papilloma viruses)

  • >40 different papilloma viruses cause warts– naked, double-stranded DNA, icosahedral capsule
  • The warts are benign growths on the epithelium of the skin or mucous membranes
  • Diagnosis is primarily clinical – typical cauliflower-like lesions on the penis, vulva or peri-anal region. Confirmed by PCR from cervical swab or biopsy
  • Treatment is removal via chemical means (podophyllin) or physical means (cryocautery)

Vaginal thrush, balanitis (Candida albicans yeast) – may be sexually transmitted

  • Approximately 75% of women will have at least one occurrence in their lifetime
  • Females have thick curd-like discharge, males usually asymptomatic
  • Predisposing factors
    • Pregnancy and oral contraceptives – leads to higher glycogen content in vaginal environment
    • Broad spectrum antibiotics – eliminates normal flora
    • Diabetes and steroids
  • Diagnosis by lower vaginal swab, wet mount, gram stain and culture on Saboraud's medium
  • Treatment only if symptomatic with topical anti-fungals; test for diabetes in males


  • Trichomona vaginalis – protozoan, 4 anterior flagella, posterior flagellum attached to undulating membrane, jerky motility
  • Site of colonization is the vagina or urethra in men
  • Women are the main carriers, up to 50% asymptomatic
  • Low prevalence in males, usually asymptomatic so important reservoir
  • Symptoms – acute inflammation, frothy foul-smelling discharge containing large numbers of PMN, causes hemorrhage on the cervix (strawberry cervix)
  • Diagnosis by high vaginal swab; examination of a wet mount, cannot be culture
  • Treatment – single dose of metronidazole or tindazole

Genital herpes

  • HSV (herpes simplex virus) 1 and 2 frequently isolated from both oral and genital sites
  • Lesions occur 3-7 days after infection, swollen lymph nodes, fever, headache, malaise; healing up to two weeks
  • Scrape of lesion collected for diagnosis
  • Diagnosis by PCR and ELISA (seroconversion can take 12 weeks)
  • No curative therapy, but anti-virals (acyclovir) may shorten episode if commenced in first 72 hours
  • Recurrences are common but generally less severe


  • Caused by Treponema pallidum, a thin coiled organism that cannot be gram stained or grown in vitro
    • Penetrates skin or mucous membranes
    • Multiplies extra-cellularly by infiltration of plasma cells PMN and macrophage
    • Painless ulcer or chancre occurs at initial site of infection (heals in 3-6 weeks if untreated)
    • Secondary syphilis occurs when organisms escape lesions, become trapped in drainage lymph nodes and multiply. Involves flu-like illness, myalgia, headache, fever, muco-cutaneous rash
    • Latent symphilis – treponemes dormant in the liver and spleen; re-awaken and multiply 3-30 years on
    • Tertiary syphilis – further dissemination and invasion; neurosyphilis, cardiovascular syphilis, progressive destructive disease
  • Congenital syphilis – mothers may transmit at any stage, leading to abortion, still birth, multiple organ failure, CNS defects, rash and jaundice; completely preventable
  • Diagnosis by dark field microscopy and direct fluorescent antibody
  • Treatment by antibiotics of benzathine penicillin; later stages of disease require long term treatment and follow up

Pelvic inflammatory disease

PID is a clinical syndrome in females associated with infection and inflammation of the upper genital tract. Affected organs include the uterus, oviducts (salpingitis), ovaries, and sometimes surrounding structures of the peritoneum

Risk factors mirror sexually transmitted diseases – young, low education and socioeconomic status, new/recent partner, vaginal douching. The majority are sexually transmitted, primarily by Neisseria gonorrhea and/or Chlamydia trachomatis. May be non-sexually transmitted post-partum, post-abortal, or post-instrumentation (operative or IUCD within 30 days), or endogenous vaginal microorganisms.

Clinical presentation Management Complications if untreated
* Varies, commonly asymptomatic
  • Classic presentation (5-10%) – severe abdominal pain, fever, vomiting
  • Mild-severe abdominal pain and tenderness
  • Vaginal/urethral discharge, may be green or yellow in colour and foul-smelling
  • Post coital bleeding
  • Dysuria
* Removal of retention products
  • Sexual partners must be notified, examined, and treated
  • Notify health department


  • CT – extended treatment as slow growing and antibiotics kill only RBs; doxycycline or roxithromycin
  • NG – ceftriaxone, plus doxycycline if chlamydia has not been ruled out
* Chronic pelvic pain
  • Infertility in approximately 20%
    • Adhesions of ovaries and oviducts
    • Tubal obstruction (tubal factor infertility) – obliteration of oviducts most commonly due to past salpingitis
  • Ectopic pregnancy
  • Recurrent PID – increased risk of permanent damage
  • Bacteraemia – suppurative arthritis, meningitis, endocarditis
  • Adhesions – intestinal obstruction

Neisseria gonorrhea, incubation 2-7 days

  • Major global disease, 60 million cases/year, notifiable disease (4000-6000 notifications/year in Australian)
  • Does not survive well outside the body as sensitive to drying
  • Higher transmission rate by men, because of high numbers of bacteria in spread
  • Development of disease:
    • N. gonorrhoeae enter host via the mucosa of the vagina, urethra, throat or rectum
    • Attach to epithelial cells of the urethra or cervix, mediated by pili and other surface proteins
    • Rapid multiplication
    • Invasion of epithelial cells for protection from phagocytes and antibodies. They multiply within vacuoles which move through the cell, fuse with the basement membrane; bacteria discharged into sub-epithelial CT
    • Localised host cell damage due to inflammatory response; however may spread to bloodstream
  • May develop as:
    • Throat infection
    • Urethral (and cervical) gonorrhea – M>90%, F<50% develop symptoms of purulent urethral discharge, severe burning and pain on urination
    • Rectal gonorrhea – M18-34%, F>95% develop symptoms of mild burning on defecation, blood in faeces, itching and mucopurulent discharge
  • Complications – bacteremia, dermatitis, gonococcal arthritis, PID (10-20%)
  • As it is asymptomatic, it is an unrecognized source of infection; 30% are untreated and spread further up the genital tract, leading to PID (salpingitis, oophoritis, peritonitis)
  • Neonatal infection – newborns exposed in birth canal, leads to blindness if untreated
  • Diagnosis by swab of discharge and direct gram stain, bacterial culture, or PCR of urine sample

Chlamydia trachomatis is divided according to serotypes

    • A, B1, B2 and C – trachoma
    • D-K – genital infection (non-specific urethritis), ocular and respiratory infection
    • L1,2,3 – systemic infection, lymphogranuloma venereum
  • Small bacterium, obligate intracellular parasite (can only grow in mammalian cell lines)
  • Complex life cycle – reticulate body (intracellular replication) and elementary body (extracellular survival)
    • Enter host via tiny abrasions in mucosal surface, growth restricted to columnar and transitional epithelium
    • EB initiates infection by binding to epithelial cell receptors on host cells
    • Parasite-specific endocytosis – fusion of chlamydia containing vesicle with lysosomes inhibited
    • Differentiation to and multiplication of RBs
    • Differentiation into EBs
    • EB progeny released into extracellular environment, and spread to adjacent cell
  • Commonly asymptomatic (F50-85%, M25-40%). Symptoms are discharge and urethritis in men
  • May lead to salpingitis – inflammation of the fallopian tubes, leading to scarring and infertility
  • Peri-natal infection via birth canal – 10-30% born to infected mothers develop purulent conjunctivitis
  • Diagnosis – first-catch urine or swab of epithelium (cervix, urethra, rectum), pus or urethral exudates inadequate; direct detection in smears, tissue cultures, ELISA or PCR

Lab diagnosis –

Neisseria gonorrhea Chlamydia trachomatis
* Gram negative diplococcus inside polymorphonuclear cells
  • Fastidious, so requires enriched media for culture
    • Chocolate Blood Agar – shows normal genital flora
    • Gonococcal (VCN) – nutrients and antibiotics specific for isolation of NG from genital tract specimens
  • Oxidase test positive
  • Carbohydrate fermentation tests
    • Positive – glucose (yellow)
    • Negative – sucrose, maltose (blue)


Obligate parasite, can only be grown in cell culture
  • Tissue culture (gold standard) – expensive, slow
  • Will not grown on CBA


  • Direct fluorescent antibody staining with monoclonal antibodies and genetic probe
  • PCR – urine, cervical swab or discharge. Does not provide information on antibiotic sensitivity, but can distinguish from gonococcol from a single specimen

Harry rides very shit cunts Maternal Infections causing congenital defects HIV Rubella Varicella Zoster virus (Group B) Streptococcus Cytomegalovirus (CMV)

How can Harry get seven hookers to tapdance? STDs

  • Human Papillomavirus
  • Chlamydia
  • Herpes simplex virus 1 and 2
  • Gonorrhea
  • Syphilis
  • Hep B and C
  • Trichomoniasis
  • Thrush