GUM Flashcards
Herpes in Pregnancy: when to c-section
Primary maternal infections, if
(a) >equal 28 weeks
(b) if <28 weeks but CS expected within the next 6 weeks.
Neonatal Herpes:
Incidence
Risk of infection infection
Incidence (2019-2022) - 6.9/100,000 live births
Transmission via contact with infected maternal secretions
Aetiology HSV-1 (52%) or HSV-2 (48%)
Greatest risk of transmission is primary infection within 6 weeks of delivery due to the absence of maternal transplacental antibodies (41% chance)
Risk of neonatal transmission:
Primary: 41%
Recurrent: 0-3%
Significant associated morbidity and mortality:
Overall mortality (all presentations of neonatal HSV) 24% - more common in premature and HSV-2
What’s new in the 2024 management of genital herpes in pregnancy guideline
· Use of ulcer panel PCR testing for herpetic lesions in pregnancy.
· Antiviral suppressive therapy to start earlier at 32 weeks of pregnancy for all mothers and pregnant people requiring this, and at 22 weeks if there is a high risk of preterm delivery.
· Use of valaciclovir as an alternative to aciclovir for treatment and/or suppression of genital herpes in the pregnant woman or person.
· A new section on the use of serology in the third trimester, and virology involvement in writing this guideline.
· Expansion of the neonatal management section, including risk stratification to guide investigations and treatment.
· Expansion of the prevention of postnatal transmission section, including a new section on breastfeeding.
· A new section on the management of clinically or serodiscordant couples
Neonatal herpes sub groups
- disease localised to only skin, eye and/or mouth (SEM)
- local central nervous system (CNS) disease (encephalitis alone or with SEM lesions)
- disseminated -disease with multiple organ involvement.
when does Neonatal infection occur?
infection at
1. the time of birth (85%),
2. in the immediate postnatal period
(10% - HSV1 only) or,
3. very rarely, in utero (5)% - termed congenital
herpes.4
Disease localised to skin, eye and/or mouth (SEM)
Mortality
Morbidity
Approx 32% of neonatal herpes cases
Median presentation at 8 days of life.
Typically present with vesicular lesions or ulcers on the skin, eye or mouth and
have no CNS or visceral organ involvement.
With appropriate antiviral treatment to prevent progression, mortality is 0% and neurological and/or ocular morbidity is around 6% and more likely in those with at least 3 lesions or HSV-2
at risk of recurrent SEM disease during childhood
Central nervous system disease/meningoencephalitis
Mortality
Morbidity
35% have CNS disease with a
Median presentation of 14 days
They may present with a variety of signs including lethargy, poor feeding, or seizures and may not have skin, eye and/or mouth lesions
With antiviral treatment, mortality from CNS disease is around 15% and more likely in those who are semi-comatose or comatose, in premature infants, and in those with delayed time to treatment.
Neurological morbidity (including developmental delay, epilepsy, blindness and cognitive disabilities) is common at 64%, and more frequent in those with seizures, HSV-2 infection, and those with delayed time to antiviral treatment
Disseminated infection
Define
%
% fever, % sepsis
Mortality
Morbidity
33% of infants with neonatal herpes have disseminated disease with a median presentation of 6 days
Multiple organs are involved and may include the liver, lungs and brain, and skin, eye and/or mouth symptoms may be absent.
Features of dissemination are typically nonspecific with only 18% presenting with fever and 79% presenting with ‘sepsis’.
Disseminated disease carries the worst prognosis – with appropriate antiviral
treatment, mortality is still around 66% and more likely in those who are semi-comatose or comatose, have HSV pneumonitis, disseminated intravascular coagulopathy, are premature, or with delayed antiviral treatment
41% of infants have long term morbidity and this is more likely in those with seizures, HSV-2 infection, or delayed antiviral
treatment
Liver, lungs, brain
33, 66, 44,
20% fever, 80% sepsis
HSV transmission
- INITIAL EPISODE (1/3rd present)
(A) PRIMARY INFECTION (first infection with either HSV-1 orHSV-2 in an individual with no pre-existing antibodies to
either type)
(B) NON-PRIMARY INFECTION first infection with either HSV-1 or HSV-2 in an individual with pre-existing antibodies to the other type.
- RECURRENT EPISODE
recurrence of clinical symptoms due to reactivation of pre-existent HSV-1 or HSV-2 infection after a period of latency.
Factors associated with transmission of neonatal herpes
Type (primary/non-primary or recurrent) and
timing of maternal infection,
The absence of transplacentally-acquired maternal neutralising antibodies
The duration of rupture of membranes before delivery,
The mode of delivery,
The use of assistance (vacuum, forceps or fetal scalp electrodes)
Syphilis on dg microscopy
Appearances of spirochaetes such as Treponema pallidum (grem neg) on dark-field microscopy:
Tightly spiralled / helically coiled / corkscrew shaped
Contain endoflagella (axial filaments)
Motile (if recent sample)
May appear straight or flexed
Congenital syphilis
Early disease (first 2 years)
Maculopapular rash (hands and feet)
Snuffles (secretions in the nose sometimes contain spirochetes)
Hepatosplenomegally
Optic neuritis
Late disease (>2 years)
Saber shins (bent tibia)
Saddle nose
Hutchinson teeth (notched teeth)
Hearing loss
Antigens on Treponema pallidum
- Group specific antigen (present on all treponemas)
- Species specific antigen (specific to T. pallidum)
- Cardiolipin (lipid antigen in spirochetes and cells in our body)
Diagnosis of syphilis: acquired
Dark field microscopy (from chancre)
Serological tests: Non-treponema tests
Detect ANTI-CARDIOLIPIN ANTIBODY (“Reagin”), not specific to syphilis
* Rapid plasmin reagin test (RPR)
* Venereal disease research laboratory test (VDRL)
Serological tests: Treponemal tests
Detect antibodies that specifically target T. pallidum
*Treponema pallidum particle agglutination test (TPPA)
*Fluorescent treponemal antibody absorbed (FTA-ABS)
Diagnosis of syphilis: congenital
- Serology:
Look at mom compared to baby
Non treponemal serological titer - CSF fluid
VDRL, cell count, protein - Long bone XR
- Eye exam
- Hearing screen
Treponema pallidum particle agglutination (TPPA) test
What is the most infective stage of syphilis?
Secondary
Latent syphilis: Early vs Late phase
Early latent: within a year of infection - spirochetes can still be found in the blood, can cause symptoms.
Late latent: after a year, tend to stay in tiny capillaries in organs/ tissues.
Tertiary syphilis: organs effected
CVS
Neurological
Liver
Joints
Testes
Tertiary syphilis: cardiovascular sequelae
Endarteritis - inflammation of the vasa vasorum (supply the aorta) - aortitis -> aortic aneurysms
Tertiary syphilis: neurosyphilis
POST SC
Inflammation in capillaries (due to presence of spirochetes) that supply posterior spinal cord - TABES DORSALIS (wasting/ loss of back of spinal cord) - loss of vibration sense, loss of proprioception.
ANT SC
Sometimes, inflammation of caps that supply anterior sc - general paresis (loss of sensation, weakness, lower limb paralysis)
BRAIN
Slurred speech, altered behaviour, memory loss, difficulty coordinating movement, paralysis
ARGYLL ROBERTSON PUPIL (pupil loses light reflex BUT does still have accommodation, so still adjust when near object)
Tertiary syphilis
Tertiary syphilis hypersensitivity reaction
Type 4 hypersensitivity reaction (lead by T cells, macrophages secrete : TNF, IL1, IL6)
Plasma cells
Type 4 hypersensitivity reaction
Types of hypersensitivity reactions
ACID
Type 1: IgE - medicated; quick onset after exposure (meds, latex)
ALLERGIC
Type 2: Ig-G mediated cytotoxic: Cells destroyed by bound ab, either by activation of compliment or by cytotoxic T cell (phagocytosis). (Rh Incompatibility in Pregnancy - hemolytic, Antiphospholipid Syndrome)
CYTOTOXIC
Type 3: Immune complex - mediated: Ag-Ab complexes are deposited in tissues, causing activation of complement which attracts neutrophils to the site (Postpartum Endometritis, SLE, PID, non-septic Post-Gonococcal Arthritis, HIV assoc GN, drug induced serum sickness like reactions, vasculitis, SJS partially)
IMMUNE COMPLEX DEPOSITION
Type 4: Delayed or cell-mediated T cell mediated. Th1 cells secrete cytokines which activate macrophafes and cytotocic t calls (Latex, nickel, contact detmatitis, tertiary syphilis, TB, endometriosis?, SDI rejection, Reactive arthritis, abacavir hypersensitivity syndrome, SJS partially)
DELAYED
MHC class II
Function: Presents exogenous antigens (e.g., from extracellular bacteria or other pathogens) to CD4+ helper T cells.
This activates the immune system to produce antibodies or recruit other immune cells.
Structure: Composed of an α-chain and a β-chain, both anchored in the membrane.
Expression: Restricted to antigen-presenting cells (APCs) like dendritic cells, macrophages, and B cells.
Antigen Source: Extracellular proteins are taken up via phagocytosis or endocytosis, processed in endosomes, and loaded onto MHC class II.
Examples: Immune response to bacterial or parasitic infections.
HLA Genes: HLA-DP, HLA-DQ, HLA-DR.
Function: Critical for:
Activation of Th cells.
Cytokine release and coordination of the immune response.
