OB 13 Infectious Disease in Pregnancy

10/04/2018 3:00-4:30 Th LDT 408

Infectious Diseases in Pregnancy Obstetrics

Sharon Faith B. Pagunsan, MD, FPOGS, FPIDSOG, FPAFP

OUTLINE I. Legend II. Basic Principles of Maternal and Fetal Immunology III. Viral, Bacterial, Protozoal and Mycotic Infections IV. Prevention Precautions for Travel V. Bioterrorism VI. Referrences

 Vertical transmission:  passage from the mother to her fetus

of an infectious agent through the placenta, during labor or delivery, or by breast feeding. Factors that may enhance risk of Neonatal Infection:  PROM common 

1. 2.

LEGEND Red with mic bullet is from recordings Blue with open book bullet is from book

 Prolonged labor  Obstetrical manipulations more than 5 internal examinations

increases the risk  INFECTIOUS DISEASES IN PREGNANCY  Factors that Influence Disease Outcome

Secondary attack rate: the probability that infection develops in

1. Maternal serological status.

a susceptible individual following known contact with an

2. Gestational age at time of infection.

infectious person.

3. Mode of acquisition. 4. Immunological status of both mother & fetus.

Maternal and Fetal Immunology  Fetal cell-mediated and humoral immunity develop by 9 to 15

Objectives:

1. To determine the basic principles of maternal and fetal immunology; 2. To identify viral, bacterial, protozoal and mycotic infections; 3. To know the prevention precautions for travel; & 4. To define bioterrorism. MATERNAL AND FETAL IMMUNOLOGY  Pregnancy-Induced Immunological Changes

weeks’ gestation.  Immunoglobulin M (IgM) - primary fetal response to

infection.  Passive immunity - IgG (transferred across the placenta), rapid

increase by 16 weeks AOG.  By 26 weeks  fetal concentrations = mother’s concentration  After birth, breast feeding is protective against some

infections  decline at 2 months of age. where does the newborn get these protective factors? Through the colostrum,

Even after intensive study, many of the maternal immunological adaptations to pregnancy are not well elucidated. It is known that pregnancy is associated with an increase increase in CD4-positive T cells secreting T2-

type cytokines - for example interleukins interleukins 4, 5, 10, and 13. Th1-type cytokine production - for example, interferon gamma and interleukin 2 - appears to be somewhat suppressed, leading to a Th2 bias in pregnancy. This bias afects the ability to rapidly eliminate certain intracellular pathogens during pregnancy, although the clinical implications of this suppression are unknown. Importantly, the T2 humoral immune response remains intact .  Horizontal Horizontal trans trans miss ion:  spread of an infectious agent from

one individual to another.

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it can protect the baby upto 6 months if exclusively breastfed  breastfeeding for the first 6  WHO recommendation: “exclusive breastfeeding months of life with partial breastfeeding until 2 years of age” feeding bottles are not allowed in BF friendly hospitals 

 Infections < 72 hours after delivery  most often caused by

bacteria acquired in utero or during delivery.  Infections after 3 days  believed to be acquired after

delivery.

 Secreted into all body fluids t ransmitted by person-to-person

contact with viral-laden saliva, semen, urine, blood, & nasopharyngeal nasopharyngeal and cervical secretions. Maternal Infection

,Zika

 Seronegative women before pregnancy are at greatest risk to

have an infected fetus.  Most CMV infection are clinically silent but can be detected

by seroconversion. seroconversion.  Diagnosis in non primary infection is a challenge.  Pregnancy does not increase the risk or severity of maternal

CMV infection.  Most infections are asymptomatic.

Mononucleosis-like syndrome: fever, pharyngitis,  Mononucleosis-like lymphadenopathy, lymphadenopathy, and polyarthritis. Immunocompromised women: myocarditis, pneumonitis,  Immunocompromised hepatitis, retinitis, gastroenteritis, or meningoencephalitis. meningoencephalitis.  Primary infection: ↑ serum aminotransferases or

lymphocytosis.  Reactivation is asymptomatic, although viral shedding is

common.  Transmission rates:

Signs of Neonatal Infection: vomiting,  In Utero: depression & acidosis at birth, poor suck, vomiting, or abdominal distention, respiratory insufficiency, lethargy or

maternal infections infects the fetus in only 0.15 to  Recurrent maternal

 jittery.  Sepsis: hypothermia &

 total leukocyte & neutrophil

1 % of cases.  Naturally acquired immunity during pregnancy  70% risk

counts. although

1st trimester  – 30-36% nd  trimester  – 34-40% o2 rd o 3  trimester  – 40-72% o

it can also present hyperthermia and/or increased

total leukocyte and neutrohil counts 

reduction of congenital CMV infection in future pregnancies  Maternal immunity does not prevent recurrences, and

maternal antibodies do not prevent fetal infection. there is VIRAL INFECTION  Cytomegalovirus

Enteroviruses: Coxsackievirus  Enteroviruses:

 Varicella-Zoster Virus

and Poliovirus

 Influenza

 Parvovirus

 Mumps

 West Nile Virus

 Rubeola – Measles

 Corona Virus Infections

 Rubella – German

 Ebola Virus

Measles

 Zika Virus

 Respiratory Viruses

no such thing as immunity in CMV because it can recur but it can reduce the risk  Fetal Infection  Symptomatic CMV infection: when a newborns has apparent

sequelae of in-utero-acquired CMV infection.  Congenital infection is a syndrome: growth restriction,  , intracranial calcifications, chorioretinitis, mental and motor

retardation, sensorineural deficits, hepatosplenomegaly, hepatosplenomegaly,  jaundice, hemolytic hemolytic anemia, & thrombocytopenic purpura.

 Hantaviruses

CYTOMEGALOVIRUS (CMV)  A ubiquitous DNA herpes virus.

common perinatal infection infection in the developed world.  Most common

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 High anti-CMV IgG avidity indicates primary maternal

infection >6 months before testing.  Viral culture may be useful; a minimum 21 days is required

before findings are considered negative. only performed at Resarch Institute for Tropical Medicine (RITM)   Modalities: Ultrasound, CT scan, & MRI.

ventriculomegaly, and cerebral  Findings: microcephaly, ventriculomegaly, calcifications; ascites, hepatomegaly, splenomegaly, and hyper-echoic bowel; hydrops; and oligohydramnios.  CMV nucleic acid amplification testing (NAAT) of amnionic

fluid: the gold standard  for the diagnosis of fetal infection.  Sensitivities ranged from 70-99% depending on

amniocentesis timing.  Sensitivity: highest when performed at least 6 wks after

maternal infection  and  and after 21 weeks’ gestation .  Negative result from amnionic fluid polymerase chain

reaction (PCR) testing does not exclude fetal infection and may need to be repeated if suspicion for fetal infection is Sagittal (A) and coronal (B) cranial sonograms from a neonate with congenital cytomegalovirus cytomegalovir us infection. The arrows indicate periventricula periventricularr calcifications.

high. Management and Prevention

 Of the estimated 40,000 i nfected neonates born each year,

only 5 to 10 percent demonstrate the syndrome. syndrome.  Most infected infants are asymptomatic at birth, but some

develop late-onset sequelae.  Complications: hearing loss, neurological deficits,

chorioretinitis, psychomotor retardation, and learning disabilities.  In dichorionic twins, infections most likely are nonconcordant.

Prenatal Diagnosis  Routine prenatal CMV serological screening is currently NOT

recommended.  Pregnant women should be tested if they present with a

mononucleosis-like illness or if congenital infection is suspected based on abnormal sonographic findings  during  during prenatal work ups.  CMV-specific IgG testing (of paired acute and convalescent

sera) - used to d iagnosed primary infection.  CMV IgM does not accurately reflect timing of seroconversion

 With primary or recurrent CMV: management is limited to

symptomatic treatment.  If recent primary infection is confirmed, amnionic fluid

analysis should be offered.  Counseling depends on the gestational age primary infection

is documented.  Currently, no proven treatments are available.  Valacyclovir, 8 g daily PO, showed adverse outcomes  in

eight of eleven affected fetuses treated at 25.9 wks AOG.  Valganciclovir IV administered for 6 wks to neonates with

symptomatic CNS prevented hearing deterioration  at 6 months and possibly later.  Passive immunization with CMV-specific hyperimmune

globulin may lower the risk of congenital CMV infection.  There is no CMV vaccine.  Prevention relies on avoiding maternal primary infection, esp.

in early pregnancy. advise the mothers not to go to crowded places such as malls 

because IgM antibody levels may be elevated for more than a

 Basic measures: good hygiene & hand washing.

year.  just because IgM is still there/elevated there/elevated it doesn’t doesn’t mean

 CMV may be sexually transmitted among infected partners,

that the mother just had the infection 

but no data address the efficacy of preventive strategies.

 CMV IgM may be found with reactivation disease or

reinfection with a new strain. CPU College of Medicine | Medentes Cum Corde| 2020 | Group 4

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VARICELLA ZOSTER VIRUS (VZV)

a double-stranded DNA herpesvirus



acquired during childhood



90% of adults have serological evidence of immunity



82% decline after the introduction of varicella vaccination

Congenital varicella syndrome rarely develops

o



 drop

in cases of maternal herpes zoster Zoster is contagious if blisters are broken,

o

although less so than primary varicella.

in maternal and fetal

Fetal and Neonatal Infection

varicella rates



first half of pregnancy  may develop congenital varicella syndrome

Primary Infection (varicella ( varicella or chicken pox)  



Features

transmitted by direct contact with an affected individual through respiratory transmission



incubation period: 10 to 21 days



nonimmune woman has a 60 to 95% risk of becoming infected after exposure

Maternal Infection

o

Chorioretinitis

o

Microphthalmia

o

cerebral cortical atrophy

o

growth restriction

o

hydronephrosis

o

limb hypoplasia

o

cicatrical skin lesions



1 to 2 day flulike prodrome



Highest risk: Between 13 & 20 weeks



followed by pruritic vesicular lesions that crust over in



After 20 weeks gestation: No clinical evidence of

3 to 7 days

congenital infection



tends to be more severe in adults



affected patients are more contagious from day 1



weeks (between 13 & 20 weeks) 

before the onset of rash until the lesions become



crusted 

Sporadic reports: CNS abnormalities & skin lesions (21 to 28 weeks of gestation)

Mortality is due to VZV pneumonia



more severe during adulthood and particulary

o

in chicken pox, highest risk is also in the earliest

If the fetus or neonates is exposed to active infection just before or during delivery (before

in pregnancy

maternal antibody has been formed)

 serious



2 - 5% develop pneumonitis



Risk factors: smoking & > 100 cutaneous cutaneous lesions



Mortality rates - 30 %



Symptoms of pneumonia - appear 3 to 5 days into the



Disseminated visceral and CNS disease which is

threat to newborns

course of illness

commonly fatal

fever, tachypnea, dry cough, dyspnea, &

o



pleuritic pain

o

Nodular infiltrates are similar to other viral

o

should be administered to neonates born to mothers who have clinical evidence of varicella

pneumonias 

Varicella-Zoster Immune globulin

5 days before and up to 2 days after delivery

Although resolution of pneumonitis parallels that of

 this

immune globulin is very difficult to acquire 

skin lesions, fever and compromised pulmonary function may persist for weeks 

If reactivated years later

 

causes Herpes Zoster or

Shingles  o

usually clinical



may be isolated by scraping the vesicle base during primary infection



Zoster is contagious if blisters are broken  just

o



a unilateral dermatomal vesicular eruption associated with severe pain

o

Diagnosis of VZV

like varicella  varicella 

antibody testing 

Zoster does not appear to be more frequent or severe in pregnant women

Tests: Tzanck smear, smear, tissue culture, or direct fluorescent Confirmation of vesicular fluid by Nucleic Acid Amplification Tests (NAATs) which (NAATs) which are very sensitive



Congenital varicella analyzed through NAAT analysis of amniotic fluid

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Page 4 of 17





A positive result does not correlate well with the

who may become pregnant within a month

development development of congenital infection

following each vaccine dose.

Sonographic evaluation: At least 5 weeks after maternal

Attenuated vaccine virus is not secreted in breast

o

infection may disclose abnormalities but the sensitivity is

milk

low

Postpartum vaccination of mothers should not b e

o

delayed because of breast feeding Management of VZV 

Maternal Viral Exposure Exposed gravid with no history for chicken pox

o

should Undergo VZV serologic testing 

INFLUENZA 

caused by members of the family Orthomyxoviridae 



Influenza A and B - form one genus of these RNA viruses

At least 70 percent of these women will be seropositive, and thus immune



immune globulin) 

best within 96 hrs (4 hrs (4 days) of exposure

to cause epidemic human disease

Influenza A viruses – subclassified by hemagglutinin (H) & neuraminidase (N) surface antigens

If susceptible: Give VariZIG (varicella zoster

o

 known



Influenza outbreaks occur annually



Most recent epidemic (2016-2017) ( 2016-2017) – Influenza A/H3N2 strain

(approved for up to 10 days) to prevent or attenuate varicella infection 

Maternal Infection Any patient diagnosed with primary primary varicella

o

Maternal and Fetal Infection 

symptoms

infection or herpes zoster should be isolated from

o

pregnant women o

a chest radiograph is recommended

o

Supportive care is given

o

Hospitalization only for those who require IV fluids and w/ pneumonia 







deaths 



Higher rates of neural-tube defects in neonates born to women with influenza early in pregnancy

Varivax 

No firm evidence that influenza A virus causes congenital malformations

Vaccination o

widespread influenza A infection affected pregnant women and caused 12 percent of pregnancy-related

ORAL, give 800 mg 5x a day during

waking hours (6am, 10am, 2pm, 6pm, 10pm)

Pregnant women - more susceptible to serious complications (i.e. pulmonary involvement)

mg/kg every 8 hours is given to women  For

An attenuated live-virus vaccine

o

Viremia is infrequent & transplacental passage is rare



Stillbirth, preterm delivery, & first- trimester abortion o

adolescents and adults with no history of varicella

o



given at 2 doses 4 to 8 weeks apart

Detected in Nasopharyngeal swabs using viral antigen rapid detection assays

Recommended Recommended for adolescents and adults

o

o

Rapid influenza diagnostic tests (RIDTs) – least indicative (sensitivities of 40-70%)

& the breakthrough infection rate approximates

o

Reverse transcriptase-polymerase chain reaction (RT-PCR) - more sensitive & specific test

Vaccine-induced Vaccine-induced immunity di minishes over time 5% at 10 years

correlated to severity of maternal infection or the flu

with no history of varicella o

This was possibly associated with hyperthermia



recommended recommended for nonpregnant



usually is not life-threatening in otherwise healthy adults

IV acyclovir - 500 mg/m² or 10 to 15 requiring hospitalization

Maternal influenza: fever, dry cough, & systemic



Decisions to administer antiviral medications for

The vaccine is not recommended for pregnant

influenza treatment or chemoprophylaxis

women ( only the immunoglobulin)  or  or for those

clinical symptoms & epidemiological factors

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 based

on

Page 5 of 17



The start of therapy should not be delayed pending

For

example: Before the end of 2018, they are starting

testing results

to produce the vaccine for 2019 since they have already predicted the strain, so you can have yourself injected   Flu

Outpatient Influenza A and B Virus Testing Methods: Method

April or May) 

Test Time

Viral cell culture

3-10 d

Rapid cell culture

1-3 d

Direct (DFA) or Indirect (IFA)

1-4 hr

vaccine is available as early as February (sometimes



Vaccination recommended: o

influenza season (optimal: Oct/Nov)  our

fluorescent antibody assay RT-PCR and other molecular

1-6 hr

o

Rapid influenza diagnostic tests

those affected by chronic medical disorders (i.e. infection)

< 30 min 

a

Nasopharyngeal Nasopharyngeal or throat swab

No evidence of teratogenicity or other adverse maternal or fetal events

Management

we

2 classes of antiviral medications:



1. Neuraminidase inhibitors  o

Inactivated vaccine: vaccine: prevents clinical illness in 70 -90 % percent of healthy adults

available in RIPF 



rainy season starts from June 

diabetes, heart disease, asthma, or HIV

assays

only

all women who will be pregnant during the

can already give as early as first trimester 

Lower rates of influenza in infants up to 6 months of age whose mothers were vaccinated during pregnancy

For early influenza A and B

o



Oseltamivir (Tamiflu) – oral & for

seasonal influenza vaccine in pregnant women

chemoprophylaxis usually



is similar to that i n the nonpregnant individual

given 



Zanamivir (Relenza) – inhaled

o

women

Peramivir (Rapivab) - IV

2. Adamantanes –  Adamantanes – Amantadine Amantadine & Rimantadine

A live attenuated influenza virus is available for intranasal use but not recommended for pregnant

contraindicated 



Immunogenicity Immunogenicity of the trivalent inactivated

MUMPS

influenza A resistance to adamantine was reported to exceed 90 percent in the United States. Thus, its use is not not currently



Uncommon adult infection - caused caused by RNA paramyxovirus paramyxovirus



Primarily infects salivary glands mumps (Latin, “to grimace”)



May involve: involve: gonads, meninges,pancre meninges,pancreas as

recommended. It is possible that that these drugs may again be effective for subsequently mutated strains. 

Limited experience with all the antiviral agents in pregnant women



 Especially



FDA category C drugs (use drugs  (use when the potential benefits Start oseltamivir treatment within 48 hours, 75 mg BID PO x 5 days



Prophylaxis: 75 mg OD PO x 10 days



Antibacterial medications added when secondary bacterial pneumonia is suspected

Vaccination 

Effective vaccines - formulated annually the

Transmitted by direct contact: respiratory secretions, saliva, or through fomites.

outweigh the risks) 

males



Treatment is symptomatic



mumps during pregnancy is no more severe than in nonpregnant nonpregnant adults.



Mumps in the first trimester risk of spontaneous abortion



Not associated with congenital malformations & fetal infection is rare.

strain of flu is already predicted for that year

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Vaccination 

Live attenuated Jeryl-Lynn vaccine strain is part of the MMR



Breastfeeding is not contraindicated



Increased rates of spontaneous abortion, preterm delivery,

vaccine (measles,mumps, & rubella) – contraindicated in

& low-birthweight neonate.

pregnancy. 



No malformations to MMR in pregnancy but pregnancy

if a woman develops measles shortly before birth risk of serious infection developing in the neonate.

should be avoided for 30 days after mumps vaccination. RUBELLA (GERMAN MEASLES)

We do not plan to give it if there is a plan to get get pregnant for



at least a month.

RNA togavirus - causes infections of minor importance in the absence of pregnancy. Rubella infection in the first trimester -poses significant risk for



Vaccine may be given to susceptible women postpartum



Breast feeding is not a contraindication.

 We

advise giving MMR before mother is discharged after

delivery.

abortion & severe congenital malformations Transmission - via nasopharyngeal secretions. Peak incidence - late winter & spring Maternal rubella infection infection - mild, febrile illness with generalized

RUBEOLA (MEASLES)

maculopapular rash beginning on face & spreading to trunk &



Caused by RNA virus of the f amily Paramyxoviridae

extremities



Annual outbreaks - late winter & early spring

Other symptoms: arthralgias or arthritis, head & neck

Transmission - primarily by respiratory droplets Characterized Characterized by: fever, coryza, conjunctivitis, & cough. Characteristic 

erythematous maculopapular rash – face & neck, spreads to

lymphadenopathy, lymphadenopathy, & conjunctivitis Incubation period – period – 12-23 days 

Viremia precedes clinical signs by a week



Adults are infectious during viremia & through 7 days after the rash appears

back, trunk, & extremities. 

Koplik spots   - small white lesions with surrounding



viremia that may cause devastating fetal infection.

erythema - oral cavity.

Diagnosis

Diagnosis 

by serology; RT-PCR tests.



but we can diagnose diagnose clinically 

Treatment

Isolated from urine, blood, nasopharynx, & CSF up to 2 weeks after rash onset. Diagnosis –  with  with serological analysis 

Pregnant women - IV immune globulin (IVIG), 400 mg/kg within 6 days of a measles exposure.

up to 6 wks after appearance of rash). 

Rubella virus infection transient low levels of IgM.



Serum IgG antibody peak 1-2 wks after rash onset.



IgG avidity testing performed concomitant with the serological tests.

Vaccination   - not performed not performed during pregnancy 

Susceptible women can be vaccinated routinely postpartum

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Specific IgM antibody detected using enzyme-linked immunoassay 4-5 days after onset of clinical disease (persist

Treatment is supportive



Up to a half of maternal infections are subclinical despite

High-avidity IgG antibodies indicate infection at least 2 mos in the past. Page 7 of 17

Fetal Effects





One of the most complete teratogens.



A sequelae of fetal infection are worst during organogenesis

MMR vaccine should be offered to nonpregnant women of childbearing age.



Vaccination of all susceptible hospital personnel who might be exposed to patients with rubella or have contact with

Usually first trimester 





pregnant women.

Pregnant women with rubella infection & a rash during first 12 wks AOG congenital infection in 90 %.



Rubella vaccination should be avoided 1 month before or during pregnancy.



13-14 wks AOG gestation – 50%



End of 2nd trimester – 25%



Defects rare after 20 wks AOG



Neonates born with congenital rubella may shed the virus



for many months thus a threat to other infants &

No observed evidence that the vaccine induces malformations



Prenatal serological screening for rubella is indicated for all pregnant women.



susceptible adults.

Women found to be nonimmune should be offered MMR vaccine postpartum.

If they have possible Rubella, they should be isolated.



Congenital rubella syndrome includes

RESPIRATORY VIRUSES

one or more of the following:



> 200 antigenically distinct respiratory viruses cause the common cold, pharyngitis, laryngitis, bronchitis, &

• Eye defects - cataracts & congenital glaucoma • Heart disease - PDA & pulmonary p ulmonary stenosis

pneumonia 

common cold.

• Sensorineural deafness - most common single defect





self-limited

DNA-containing adenovirus - produce cough & lower respiratory tract involvement including pneumonia.

• Pigmentary retinopathy, microphthalmia • Neonatal purpura

RNA-containing rhinovirus & coronavirus illness: rhinorrhea, sneezing, & congestion

• CNS defects - microcephaly, microcephaly, developmental delay, mental retardation, & meningoencephalitis

Rhinovirus, coronavirus, coronavirus, & adenovirus - major causes of



Amnionic fluid viral PCR studies – sensitive for adenovirus (virus most frequently identified)

• Hepatosplenomegaly & jaundice 

• Radiolucent bone disease Management and Prevention 

No specific treatment



Droplet precautions for 7 days after onset of rash are



hydrops, foot/hand abnormalities, & neural-tube defects 

Adenoviral infection - known cause of childhood myocarditis.

HANTAVIRUS 

RNA viruses - members of the family B unyaviridae

recommended



Associated with a rodent reservoir.

Postexposure passive immunization may be of benefit if



Transmission involves inhalation of virus excreted in rodent urine and feces.

given within 5 days of exposure. 

Association with fetal-growth restriction, nonimmune

To eradicate rubella & prevent congenital rubella syndrome - comprehensive approach is recommended for immunizing



Outbreaks include Sin Nombre virus and Seoul virus, most recent in early 2017.

the adult population.

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Hantavirus pulmonary syndrome syndrome - cause

maternal death,

fetal demise, and preterm birth. 



The B19 virus can cause Eryhtema infectiosum of fifth disease 



Small, single-stranded DNA virus that replicates in rapidly proliferating cells, e.g. erythroblast precursors.



Anemia is the primary fetal effect



Only individuals with erthrocyte globoside membrane P antigen are susceptible

NO evidence of VERTICAL TRANSMISSION of the causative Sin Nombre virus.

ENTEROVIRUSES 

ENTEROVIRUSES (PARVOVIRUSES)

A major subhroup of RNA picornaviruses, picornaviruses, coxsackievirus, poliovirus and echovirus.



Without EGMPA, you are least likely to be infected 



Trophic for intestinal epithelium but can cause maternal, fetal and neonatal infections.



Main mode of transmission : respiratory or hand-to-mouth contact



May include CNS, skin, heart and lungs





Most maternal infections are subclinical yet be fatal to the fetus-neonate.

Maternal infection is the highest with school-aged children and day-care workers



Viremia appears 4-14 days after exposure



Hepatitis A is an enterovirus





Coxsackie infections : group A and B are usually asymptomatic

Immunocompetent Immunocompetent individuals is no longer i nfections at the onset of the rash



Maternal infection :



Symptomatic infections - usually with group B include : o

Aseptic meningitis, polio-like illness, hand, foot and mouth disease, pleuritis, pericarditis, myocarditis

No treatment or vaccinaiton is available



May be transmitted by maternal secretions at delivery



Transplacental Transplacental passage has been reported



20-30% if adults - asymptomatic

o

Viremic phase : Fever. Headache, flu-like symptoms

o





o

 o

Congenital malformation rates slightly increased in pregnant women with serological evidence of coxsackievirus coxsackievirus

o

Viremia leads to fetal hepatitis, skin lesions, myocarditis and enchephalomyelitis enchephalomyelitis - ALL FATAL

o

o

ENTEROVIRUSES (POLIO VIRUSES) 

Highly contagious but subclinical or mild



Trophic for the CNS and can cause paralytic poliomyelitis

o



Pregnant women - more susceptible and higher death rate

o



Perinatal transmission occurs during the 3 rd trimester



Inactivated subcutaneous subcutaneous polio vaccine is recommended for susceptible pregnant women who must travel to endemic areas.

o

Live oral polio vaccine is used for mass vaccination during pregnancy without harmful fetal effects

o

Rash becomes lacelike and spreads to the trunk and extremities Adults - milder rashes and symmetrical polyarthralgia With recovey, IgM antibody is generated 7-10 days postinfection Several days after IgM is produced, IgG antibody i s detectable and persists for life with natural immunity

Vertical transmission occurs Asscoiated with : abortion, nonimmune hydrops and stillbirth Fetal loss - 8-17% before 20 weeks of gestation and 26% after midpregnancy Critical for development of fetal hydrops - between 1316 weeks of gestation

Diagnosis and management - Parvovirus 

CPU College of Medicine | Medentes Cum Corde| 2020 | Group 4

Emphasized 

Fetal infection :





Several days later, a bright red rash with erythroderma affects the face ( slapped-cheek appearance)

Fetal and maternal viral loads do not predict fetal morbidity and mortality

Page 9 of 17



Most cases, hydrops develop in the first 10 weeks after infection -> Serial sonography every 2 weeks in women wi th recent infection.



Depending on gestational age, fetal transfusion for hydrops may improve outcome



30% mortality in hydropic fetuses without transfusion



With transfusion, 94% of hydrops resolve within 6-12 weeks and decreases overall mortality rate below 10% Usually patients with hydrops are associated with Parvovirus 





DEET - considered safe for use among pregnant women



Recommendations Recommendations : avoiding outdoor activity and stagnant water, wearing PPEs.



Adverse effects of viremia of pregnancy are unclear



Transmission through breastfeeding - RARE

CORONA VIRUS INFECTIONS 

Single-stranded RNA viruses prevalent worldwide



Case fatality rate - 10% in nonpregnant, 25% in pregnant women



2002 - a virulent strain of coronavirus - Severe acute respiratory syndrome or SARS was first noted in China.



Rapidly spread throughout Asia, Europe, North and South America.



Transmission is through droplets or contact with infected secretions, fluids and wastes



Incubation period : 2-16 days with triphasic pattern to its clinical progression



Symptoms :

Parvovirus - Prevention 

No Parvovirus vaccine is available



No evidence suggests that antiviral treatment prevents maternal or fetal infections



Pregnant women should be counseled for risks of infection : o

5% for casual, infrequent contact

o

20% for intense, prolonged work exposure

o

And 50% for close, frequent interaction

o

WEST NILE VIRUS 

Mosquito-borne RNA flavivirus - a human neuropathogen o



Most common cause of arthropod-borne viral encephalitis in the United States o





Typically acquired through mosquito bites or through blood transfusion



o

Most have mild or no symptoms



Symptoms : o

Fever

o

Mental status change

o

Muscle weakness

o

Coma

Diagnosis and Management - West Nile Virus 

Clinical symptoms and detection of viral IgG and IgM in serum and IgM in cerebrospinal fluid



No effective antiviral treatment



Management Management : supportive



Primary strategy for prevention - use of insect repellant cotaining N. N-diethyl-m-toluamide ( DEET)

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2nd week : recurrent fever, watery diarrhea, dry nonproductive cough with mild dyspnea 3rd week : at times, lethal phase - seen in about 20% of patients which can progress to SARS

Radiographic lung findings:

Incubation period - 12-14 days



1st week : Prodromal symptoms of fever, myalgias, headache and diarrhea

Ground glass opacities and airspace consolidations ( Can rapidly progress 1-2 days)



No confirmed cases since 2004, CDC now lists SARS- COV as a “select agent” - potential to pose a severe threat to public health and safety



Another novel coronavirus infecting humans with a highcase fatality rate was detected in the Middle East in 2012 ( MERS-COV)

EBOLA VIRUS 

Member of the RNA Filoviridae Family



Transmitted by direct person-to-person contact



Infection causes severe hemorrhagic fever with pronounced immunosuppression immunosuppression and DIC



CDC concludes that pregnant women are more susceptible

Page 10 of 17

ZIKA VIRUS



Salmonellosis



RNA virus of the Filoviridae f amily



Shigellosis





First major mosquito-borne teratogen

Hansen Disease



Lyme Disease Tuberculosis



Primarily transmitted by mosquito bite, also by sexual transmission





Detected in body fluids for months following acute infection

Group A Streptococcus



Maternal-Fetal infection:



o

Adults - asymptomatic or mild symptoms of rash, fever, headache, arthralgia and conjunctivitis 

o

o

Streptococcus pyogenes o

important in pregnant women

o

most frequent cause of acute pharyngitis & is associated with several systemic & cutaneous

With Zika you can have a combination of your arthralgia and conjunctivitis conjunctivitis - Chikungunya arthralgia but no conjunctivitis 

infections o

responsible for the local & systemic toxicity

Virus is detectable in the blood around the time of symptoms onset and may persist for days to months in pregnant women

o

o

o

infrequent cause of puerperal infection but remains the most common cause of severe maternal postpartum infection and death and

Fetus - can be severely infected whether or not the mother is symptomatic

the incidence is rising o

o

produces numerous toxins & enzymes

Mortality - 7% in Brazil

Early 1990s rise in streptococcal toxic shock syndrome: 

With birth defects - 5% with Zika infection and 15% with laboratory-confirmed infection

hypotension, fever, & multiorgan failure with bacteremia

o

Congenital Zika syndrome :

Pyrogenic exotoxin-producing strains usually associated with severe disease

o

Microcephaly Microcephaly - Dreaded syndrome

o

Lissencephaly

o

Ventriculomegaly

o

Intracranial Intracranial calcifications

o

Occular abnormalities

o

Congenital Contractures

Diagnosis and Management - Zika Virus    

Zika virus RNA blood or urine or serological testing o PCR confirmatory o NO specific treatment or vaccine available Prophylaxis: protective netting and insect spray spray to control the vector mosquito and avoidance of sexual contact with recently exposed partners

o

Streptococcal pharyngitis, scarlet fever, & erysipelas not life threatening

o

Treatment: Penicillin similar in pregnant and nonpregnant women



Case-fatality rate approximates 30%



Morbidity & Mortality rates are improved with early recognition



Treatment: clindamycin plus penicillin therapy therapy & surgical debridement



No vaccine is commercially available

Group B Streptococcus (GBS) 

Streptococcus agalactiae o

colonize the gastrointestinal & genitourinary tract in 10-25% of pregnant women

Streptococcuss agalactiae is a group B organism that Streptococcu BACTERIAL INFECTIONS

can be found to colonize the gastrointestinal and



Group A Streptococcus

genitourinary tract in 20 to 30 percent of pregnant



Group B Streptococcus (GBS)

women. (Throughout pregnancy, group B



Methicillin- Resistant Staph aureus

streptococcuss (GBS) is isolated in a transient, streptococcu



Listeriosis

intermittent, or chronic fashion. Although the organism

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Page 11 of 17

is most likely always present i n these same women,



their isolation is not always homologous.) 

meningitis than for early-onset sepsis

Maternal and Perinatal Infection o

o

Unfortunately, it is not uncommon for

Infections range from asymptomatic

surviving infants of both early- and

colonization to septicemia

late-onset disease to exhibit

Streptococcus Streptococcus agalactiae implicated in adverse

devastating neurological sequelae.

pregnancy outcomes 

Adverse pregnancy outcomes: preterm



Prophylaxis for Perinatal Infections o

labor, PROM, clinical & subclinical

Recommendation 

chorioamnionitis, chorioamnionitis, & fetal infections o

o

osteomyelitis, postpartum mastitis, & puerperal

identified carriers Updated Guidelines (early-onset GBS) in 2010 

intrapartum chemoprophylaxis with

morbidity and mortality among infants in the

PPROM, preterm labor, or penicillin

United States

allergy & new dosing for penicillin G

Neonatal sepsis

chemoprophylaxis

the most common infection with

As GBS neonatal infections evolved beginning in the

devastating consequences

1970s and before widespread intrapartum

Early-onset disease

chemoprophylaxis, chemoprophy laxis, rates of early-onset sepsis ranged

Infection < 7 days after birth;

from 2 to 3 per 1000 live births. In 2002, the Centers

0.21/1000 live births

for Disease Control and Prevention, the American

< 72 hrs of life 

o

o

remains the leading infectious cause of



o

for GBS at 35-37 wks AOG followed by intrapartum antibiotic prophylaxis for



o

universal rectovaginal culture screening

GBS cause maternal bacteriuria, pyelonephritis, infections

o

Mortality rate less for late-onset

College of Obstetricians and Gynecologists, and the

most compatible with intrapartum i ntrapartum

American Academy of Pediatrics revised guidelines for

acquisition of disease & several

perinatal prevention of GBS d isease. They

unexpected intrapartum stillbirths

recommended recommende d universal rectovaginal culture screening

newborns with early-onset GBS

for GBS at 35 to 37 weeks’ gestation followed by

infection often had clinical evidence of

intrapartum antibiotic prophylaxis for women

fetal infection during labor or at

identified to be carriers. Subsequent to

delivery.

implementation of these guidelines, the incidence of

S epticemia epticemia

early-onset GBS neonatal sepsis has decreased to 0.24



serious illness within 6-12hrs of birth

cases per 1000 live births by 2012 (Centers for



Respiratory distress, apnea, & HOPN

Disease Control and Prevention, 2013a). These guidelines were updated for early-onset GBS infection

At the outset, therefore, neonatal infection must be

in 2010. They expanded expanded laboratory identification identification

differentiated from respiratory distress syndrome

criteria for GBS; updated algorithms for screening and

caused by insufficient surfactant production of the

intrapartum chemoprophylaxis chemoprophylaxis for women with

preterm neonate (Chap. 34, p. 653). The mortality rate

preterm prematurely ruptured membranes, preterm

with early-onset disease has declined to

labor, or penicillin allergy; and described new dosing

approximately 4 percent, and preterm newborns are

for penicillin G chemoprophylaxis chemoprophylaxis..

disparately affected. o

Late-onset disease 

manifests as meningitis 1 week to 3

o

Culture-Based Approach: 

Screening 35-37 wks gestation



intrapartum antimicrobials given with

months after birth seen in 0.32 per 1000 live births

RV GBS-positive cultures 

Prophylaxis for history of previous sibling with GBS invasive disease

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Page 12 of 17

identification of GBS bacteriuria in the

1000 live births births (Wendel, 2002). 2002). Non-GBS early-onset

current pregnancy

sepsis was identified in 0.24 per 1000 live births, and this

The 2010 Centers for Disease Control and Prevention GBS

was stable during the past two decades (Stafford, 2012).

Guidelines recommend a culture-based approach. Such a

Thus, this approach has results similar to those reported

protocol was also adopted by the American College of

by the Centers for Disease Control and Prevention (2010)

Obstetricians and Gynecologists (2013c). This approach is

for culture-based prevention.)



designed to identify women who should be given intrapartum antimicrobial prophylaxis. prophylaxis. Women are are screened for GBS colonization at 35 to 37 weeks’ gestation,

Regimens for Intrapartum Antimicrobial Prophylaxis for Perinatal GBS Disease:

and intrapartum antimicrobials are given to women with rectovaginal GBS-positive cultures. Selective enrichment enrichment broth followed by subculture improves improves detection. detection. In

Regimen

Treatment

Recommended Recommended

Penicillin G, 5 MU IV initial dose, then 2.5-3.0 MU IV

addition, more rapid techniques such as DNA probes and nucleic acid amplification tests are being developed (Chan, 2006; Helali, Helali, 2012). A previous sibling with GBS invasive

Q4H until delivery Alternative

Ampicillin, 2g IV initial dose, then 1g IV Q 4H or 2g Q6H

disease and identification of GBS bacteriuria in the current

until delivery

pregnancy are also considered indications for prophylaxis. o

Risk-Based Approach 

Recommended Recommended for women in labor with unknown GBS culture results



Risk factors: factors: delivery < 37 37 weeks, ruptured membranes > 18 hours, or intrapartum temperature > 100.4 F (> 38.0C)



Parkland Hospital (1995 - prior to consensus guidelines) all term neonates were given aqueous penicillin G, 50,000 to 60,000 units IM

A risk-based approach is recommended for women in

Penicillin allergic: Patients not at high risk for

Cefazolin, 2g IV initial dose,

anaphylaxis

then 1g IV Q 8H until deliver

Patients at high risk for

Clindamycin, 900mg IV Q 8H

anaphylaxis & with GBS

until delivery

susceptible to clindamycin Patients at high risk for

Vancomycin, 1g IV Q 12H

anaphylaxis & GBS resistant

until delivery

to clindamycin or susceptibility unknown 

o

labor and whose GBS culture culture results are not not known. This approach relies on risk factors associated with intrapartum GBS transmission. transmission. Intrapartum

> 18 hours, or intrapartum temperature > 100.4 F (>

Antibody-producing vaccines have been tested but NONE are clinically available



Intrapartum antimicrobial prophylaxis o

chemoprophylaxis chemoproph ylaxis is given to women who have any of the following: delivery < 37 weeks, weeks, ruptured ruptured membranes

GBS vaccine

Preventive antimicrobials administered 4 or

more hours before delivery are highly effective Penicillin remains the first-line for prophylaxis

38.0C). (Women with GBS during the current current pregnancy pregnancy and women with a prior infant with invasive early-onset GBS disease are also given chemoprophylaxis.) At Parkland Hospital in 1995--and prior to consensus

Methicillin-Resistant Staphylococcus Staphylococcus aureus 

Staphylococcus aureus  o

guidelines— guidelines —we adopted the risk-based approach for intrapartum treatment of women women at high risk. risk. In

staphylococcal species o

addition, all term neonates who were not given

intramuscularly. intramuscu larly. (Rates of early-onset GBS infection and and

colonizes 

intrapartum prophylaxis were treated in the delivery room with aqueous penicillin G, 50,000 to 60,000 units

pyogenic G+ organism; most virulent of the

nares, skin, genital tissues, & oropharynx

o

20% persistent carriers

o

30-60% intermittent carriers

sepsis and of non-GBS sepsis decreased to 0.4-0.66 per CPU College of Medicine | Medentes Cum Corde| 2020 | Group 4

Page 13 of 17

o





Colonization o



20-50% noncarriers

MRSA infections

greatest risk factor for infection i nfection

Methicillin-resistant S. aureus (MRSA) o

colonizes only 2 percent of adults but a

Listeriosis 

Listeria monocytogenes o

significant contributor to the health-care MRSA infections associated with  cost & higher



Community-associated Community-associated MRSA (CA-MRSA) o

when identified in an outpatient setting or



Thought to be food-borne



Outbreaks

within 48 hours of hospitalization 



Risk factors:

o

raw vegetables

o

coleslaw

o

prior MRSA infection

o

apple cider

o

hospitalization

o

melons

o

dialysis or surgery within the past year

o

milk

o

indwelling catheters or devices (w/in the past

o

fresh Mexican-style cheese

year)

o

smoked fish

o

processed foods

Hospital-associated MRSA (HA-MRSA) o

are nosocomial.



During pregnancy may be asymptomatic or may cause a

Community-associated Community-ass ociated MRSA (CA-MRSA) ( CA-MRSA) is diagnosed d iagnosed

febrile illness confused with influenza, pyelonephritis, or

when identified in an outpatient setting or w ithin 48

meningitis

hours of hospitalization in a person without traditional



hospitalization, dialysis or surgery within the past year,



cases of MRSA in pregnant women are CA-MRSA.

NO vaccine available



Prevention o

o

drainage & local wound care

Severe superficial infections 

should be treated with MRSA-

Salmonellosis 

empiric treatment for CA-MRSA until





o

linezolid 

o

o

expensive

doxycycline, minocycline, & tetracycline 



contraindicated contraindicated in pregnancy

Non-typhoid Salmonella gastroenteritis o

most are sensitive to TMP-SMZ and clindamycin

Six serotypes including Salmonella subtypes typhimurium & enteritidis  & enteritidis 

culture results are available CA-MRSA

a major & increasing cause of food- borne illness

Purulent cellulitis 

o

Infections from Salmonella species o

appropriate antibiotics o

washing raw vegetables and cooking all raw food

Uncomplicated superficial infections 

Ampicillin plus Gentamicin or TMP-SMZ



Management o

blood culture

Treatment o

and indwelling catheters or devices. Hospital-associated MRSA (HA-MRSA) (HA-MRSA) infections are nosocomial. nosocomial. Most

Diagnosis o

risk factors. The latter include include prior MRSA infection, infection,



Uncommon but probably underdiagnosed cause of neonatal sepsis

mortality rates 

facultative, intracellular Gm+ bacillus from feces of 1 to 5% of adults

burden 

first-line therapy for inpatient serious



contracted through contaminated food

Symptoms: o

nonbloody diarrhea

o

abdominal pain

o

fever

o

chills

o

nausea & vomiting (6-48hrs after exposure)

vancomycin

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Page 14 of 17

Infections from Salmonella species continue to be a



major and increasing cause of food-borne illness (Peques, 2012). 2012). Six serotypes account account for most most cases in

Relatively common highly contagious cause of inflammatory exudative diarrhea in adults



the United States, including Salmonella subtypes

Shigellosis o

typhimurium and enteritidis . Non-typhoid Salmonella gastroenteritis is contracted through contaminated food.

centers 

Symptoms including nonbloody diarrhea, abdominal pain, fever, chills, nausea, and vomiting begin 6 to 48 



o



fecal-oral route

Clinical manifestations o

mild diarrhea to severe dysentery

Diagnosis

o

bloody stools

o

abdominal cramping

o

tenesmus

o

fever

o

systemic toxicity

stool studies

IV crystalloid o



Transmission

hours after exposure.

o



more common in children attending day-care

for rehydration

Antimicrobials o

not given in uncomplicated infections

Bacillary dysentery caused by Shigella is a relatively

o

If complicated by bacteremia antimicrobials are

common, highly contagious cause of inflammatory

given

exudative diarrhea diarrhea in adults. Shigellosis is more more

Typhoid fever

common in children attending day-care centers and is

o

caused by Salmonella typhi

transmitted via the fecal-oral route. Clinical

o

Transmission: oral ingestion ingestion of contaminated contaminated

manifestations range from mild diarrhea to severe

food, water, or milk

dysentery, bloody stools, abdominal cramping,

o

Antepartum typhoid fever

 abortion,

preterm

labor, & maternal or fetal death

tenesmus, fever, and systemic toxicity. 

Typhoid fever caused by Salmonella typhi remains a global health problem, although it is uncommon in the

Self-limited o



treatment of dehydration is essential

Antimicrobial therapy

United States. Infection is spread spread by oral ingestion ingestion of

o

Imperative

contaminated food, water, or milk. In pregnant women, women,

o

include fluoroquinolones, ceftriaxone, or

the disease is more likely to be encountered during epidemics or in those with HIV infection (Hedriana,

azithromycin 

Can stimulate uterine contractions and cause preterm

1995). In former years, years, antepartum typhoid fever

birth

resulted in abortion, preterm labor, and maternal or

Although shigellosis may be self-limited, careful

fetal death (Dildy, 1990).

attention to treatment of dehydration is essential in

o

Treatment: Fluoroquinolones & 3rd generation cephalosporins

o

o

For enteric (typhoid) fever

 antimicrobial

severe cases. We have cared for pregnant women in whom secretory diarrhea exceeded 10 L/day! Antimicrobial therapy is imperative, and effective

susceptibility testing is important

treatment during pregnancy i ncludes fluoroquinolones,

Typhoid vaccines

ceftriaxone, or azithromycin. Antimicrobial resistance resistance is





no harmful effects when administered

rapidly emerging, and antibiotic susceptibility testing can

to pregnant women

help guide appropriate therapy (Centers for Disease

given in epidemic or before travel to

Control and Prevention, 2013c).

endemic areas Shigellosis 

Bacillary dysentery o

caused by Shigella

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Page 15 of 17

Protozoal Infections

Management: Prenatal treatment:

Toxoplasmosis 

Humoral and cell-mediated immune defenses eliminate



Spiramycin

most of these, but tissue cysts develop

In women with acute infection early in



pregnancy 

Two distinct stages: 



Pyrimethamin-sulfonamide Pyrimethamin-sulfonamide + folinic acid Maternal infection after 18 weeks, or if fetal

Feline stage

infection is suspected

o

In the cat (definitive host) and its prey

o

Unsporulated oocysts are secreted in the feces

Nonfeline stage Tissue

cysts

with

bradyzoites/oocysts

are

Prevention: 

No vaccine



Avoidance

ingested by intermediate host (humans) ↓

Gastric acid digests cysts to release bradyzoites

o

Cooking meat to safe temperatures;

o

Peeling/thoroughly Peeling/thoroughly washing fruits & vegetables;

o

Cleaning all food preparation surfaces &

↓

utensils that have contacted raw meat, poultry,

Small intestine epithelium infection

seafood, or unwashed fruits & vegetables;

↓ o

Transformation to tachyzoites

Wearing gloves when changing cat litter, or delegating this duty; &

↓

Infect all cells within host mammal

o

↓

Avoiding feeding cats raw or undercooked meat & keeping cats indoors

Humoral and cell-mediated immune defenses eliminate these, but tissue cysts develop

 Amebiasis

↓

Lifelong

persistence:

 Entamoeba histolytica

chronic

form

of

toxoplasmosis 

Human infection: o

Eating infected raw or undercooked meat

o

Contact with oocysts from cat feces contaminated contaminated litter, soil, water



Risks for fetal infection increases with duration of pregnancy



 Amebic dysentery: fulminant course during pregnancy with

fever, abdominal pain, & bloody stools  (+) hepatic abscess: worse prognosis  Diagnosis: identification of E. histolytica cysts or trophozoites

in a stool sample

Incidence and severity of congenital i nfection depend on fetal age at the time of maternal infection



symptomatic  Infected persons a symptomatic

o

15% at 13 weeks

o

44% at 26 weeks

o

71% at 36 weeks

Therapy: *same for preg and non-pregnant women 



If infected before 20 weeks, 11% of NB had congenital toxoplasmosis; 45% after 20 weeks



Amebic colitis & invasive disease o

Metronidazole

o

Tinidazole

Noninvasive infections o

Iodoquinol

o

Paromomycin

Severity of fetal infection is much greater in early pregnancy; fetuses are much more likely to have clinical findings of infection

Mycotic Infections 

Dilated fungal infection (usually p neumonitis) during pregnancy is uncommon with coccidioidomycosis,

Screening and diagnosis 

Prenatal screening not recommended



With IgG antibody before pregnancy, there is no risk for

blastomycosis, cryptococcosis, or histoplasmosis

congenitally infected fetus CPU College of Medicine | Medentes Cum Corde| 2020 | Group 4

Page 16 of 17

Travel Precautions during Pregnancy 



Obstetrical risks, general medical risk, & potentially

amoxicillin

hazardous destination risks 

If allergic to ciprofloxacin or



Anthrax vaccine:

International Society for Tropical Medicines and Center for Disease Control and Prevention Bioterrorism



o

Inactivated

o

cell-free product

o

3 injections over 28 days

Risk from anthrax > fetal risks from doxycycline

1.

Smallpox

2.

Anthrax

3.

Other bioterrorism agents



Francisella tularensis – tularemia



Bioterrorism involves the deliberate release of bacteria,



Clostridium botulinum – botulism

viruses, or other infectious agents to cause illness or



Yersinia pestis – plague

death



Viral hemorrhagic fevers – Ebola, Marburg, Lassa,



Other Bioterrorism Agents

Category A

These natural agents are often altered to increase their

Machupo

infectivity or their resistance to medical therapy 

Clinicians should be alert for significant increases in the

Category B&C: multiple agents

number of persons with febrile illnesses accompanied by respiratory symptoms or with rashes not easily associated with common illnesses

References  

Doc’s lecture and powerpoint William’s Obstetrics 25th Ed. Chapter 64

Smallpox 

Variola virus



Serious weapon



Highly transmissible; case fatality rate: 30%



Last case in US: 1949 Worldwide (Somalia): 1977



Vaccine is a live vaccine virus – pregnancy should be delayed for 4 weeks.

 Anthrax 

Bacillus anthracis o

Gram-positive, spore-forming, aerobic bacterium



3 main types: o

Inhalational 



2001 bioterrorist attacks

o

Cutaneous

o

Gastrointestinal

Postexposure prophylaxis (2months) o

Ciprofloxacin 500mg BID for 60 days

o

Amoxicillin 500mg TID 

Can be substituted if strain is sensitive If

o

allergic to ciprofloxacin

Doxycycline 100mg BID for 60 days

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Page 17 of 17