Infections and Infestations in pregnancy

Seminar objectives

To know the various infections and infestations that occur in pregnancy. To know their effects on pregnancy and the effects of pregnancy on them. To know the management of these conditions.

Outline

Malaria UTI Worm infestations STORCH5

Malaria

Malaria is a major cause of morbidity and mortality in children and adults particularly in the tropics It is caused by Plasmodium parasites ;

Plasmodium falciparum Plasmodium vivax Plasmodium malariae Plasmodium ovale

Plasmodium falciparum causes the severest form of malaria and is transmitted through the bite of the female anopheles mosquito Incubation period is about two weeks

Life cycle and pathogenesis

Features of uncomplicated malaria

Fever Rigors Malaise Headache Vomiting Abdominal discomfort

Features of complicated malaria

Dark-coloured urine Jaundice Drowsiness and coma Anaemia Difficulty in breathing Poor urine out put Temp 39C or more

Effects of pregnancy on malaria

Pregnant women tend to have more frequent and severe forms of malaria due to reduced immunity.

Effects of malaria on pregnancy

Placental parasitaemia Maternal anaemia Abortions Preterm birth Low birth weight Severe malaria

Effect of Malaria on the foetus

Foetal anaemia Low birth weight Pre-term delivery Still-birth Congenital malaria

Higher Risk Groups

First and second pregnancies Adolescents HIV-infected Sickle-cell disease Pregnant women from areas of low transmission

Investigations

Blood film for malaria parasites FBC If the disease is severe and diagnostic difficulties exist ,then culture of blood and urine is done to exclude enteric fever and UTI respectively.

Management of malaria in pregnancy

The Ministry of Health has adopted a threepronged approach:

Insecticide-treated nets Intermittent preventive treatment Case-management of malaria

IPT

Three doses of sulfadoxine pyrimethamine are given during ANC at monthly intervals after 16 weeks but before 36 weeks. But in Ghana, the first dose is given after 20 weeks.

Case management

For uncomplicated malaria

600mg of oral quinine tid for 7days Artesunate 2.4mg/kg bwt given iv followed by 1.2mg/kg bwt at 12hrs and 24hrs and 1.2mg/kg bwt daily for 6 days.The daily dose can be given orally if the patient is able to swallow. Arthemether 3.2mg/kg bwt given im followed by 1.6mg/kg bwt daily for 6 days. Dose can be given orally if the patient can swallow. IV quinine 10mg/kg body weight in 5% dextrose or IM quinine 10mg/kg body weight 8-hourly for 48 hours. Then continue with oral quinine for the next 5 days.

For complicated malaria

Urinary Tract Infections in Pregnancy

Introduction

UTIs are the most common bacterial infections that complicate pregnancy. In normal pregnancy, profound changes occur in the renal system. These anatomical and physiological changes influence the occurrence, progress and outcome of UTIs. The calyces, renal pelvis and ureters dilate markedly and often give the erroneous impression of obstructive uropathy. Most pregnant women show evidence of urinary stasis by the third trimester. The urinary stasis predisposes pregnant women to UTIs.

Asymptomatic Bacteriuria

It refers to the presence of actively multiplying bacteria in the urinary tract, excluding the distal urethra, in a patient without any obvious symptoms. The incidence is the same in both pregnant and nonpregnant women(2-10%). It is twice as common in pregnant women who have the sickle cell trait(AS) and 3 times as common in pregnant women who are diabetic. Organisms implicated include E. coli, Klebsiella, Staph. aureus, Group B Streptococcus and Proteus. If left untreated, 40% progress to symptomatic UTI while 30% develop acute pyelonephritis.

Effects on Pregnancy

Maternal
Anaemia PIH Preterm labour

Fetal
Low birth weight Preterm delivery

Diagnosis

Isolation of >105 organisms of the same species per ml of urine. A suitable specimen for culture and sensitivity is a clean-catch midstream specimen of urine. Other methods that may be used in obtaining the specimen of urine include suprapubic aspiration and urethral catheterization.

Treatment

The choice of drug is based on the sensitivity of the isolated organism. Ampicillin and cephalosporins can be used safely in pregnancy. Nitrofurantoin and short-acting sulfonamides may also be used. Repeat MSSU culture after treatment to ensure that the infection is cleared.

Acute Cystitis

It is a lower urinary tract infection involving the urinary bladder. It is uncommon in pregnancy. Incidence is about 1%. Organisms implicated include E. coli, Klebsiella, Staph. aureus, Group B Streptococcus and Proteus.

Signs and Symptoms

Frequency Urgency Dysuria Suprapubic pain Cloudy and offensive urine Lower back pain Haematuria

Investigations

MSSU for culture and sensitivity Urine dipstick Urine microscopy Imaging of urinary tract in recurrent cases to exclude anatomical abnormalities.

Treatment

Treatment can be on OPD basis with oral antibiotics best chosen based on culture and sensitivity results. Nitrofurantoin, ciprofloxacin, co-amoxiclav, ampicillin, trimethoprim and cephalosporins are effective. Analgesics like paracetamol may be given. Encouraging patient to drink plenty of fluids to promote good urinary output. Personal hygiene and proper cleaning after defaecation. Encouraging patient to urinate often.

Acute Pyelonephritis

It is an upper urinary tract infection involving the renal pelvis. Occurs in 1-2% of pregnant women. The risk of developing acute pyelonephritis is markedly increased in pregnancy because of obstructive uropathy and stasis of urine. Untreated asymptomatic bacteriuria adds to the risk. Organisms implicated include E. coli, Klebsiella, Staph. aureus, Group B Streptococcus and Proteus.

Signs and Symptoms

Fever (temp>38.5C) Chills Rigors Nausea Vomiting Flank pain, renal angle tenderness Headache Frequency Urgency Dysuria Dehydration

Effects on Pregnancy

Fetal

IUGR IUFD Preterm delivery

Renal failure Endotoxic shock Preterm labour Anaemia Pulmonary injury Hypothalamic instability

Maternal

Investigations

MSSU for culture and sensitivity Urine dipstick Blood for culture and sensitivity in severely ill patients Blood film for malaria parasites to rule out malaria FBC BUE, creatinine

Treatment

Admit the patient. IVFs (such as D/S and R/L) given for rehydration. Start IV antibiotics such as cephalosporins whilst awaiting the urine culture and sensitivity results. Analgesics and antipyretics such as paracetamol are given. Monitor fetal condition and watch out for preterm labour. Check urine daily for proteins and keep a BP chart. Repeat urine culture 7 days after treatment to make sure the infection is cleared.

Worm infestations

There are two main species

Ancylostoma duodenale Necator americanus (most common )

Clinical features

Ground itch at the site of entry Lofflers syndrome Anaemia Malabsorption

Life cycle

Investigations

Stool R/E for ova and occult blood Routine investigations

FBC (Hb)

Management

Anthelmintics

The Ministry of Health recommends that all pregnant women be given mebendazole(100mg bd for 3days or 500mg in the 2nd to 3rd trimester)

Ascariasis

Mode of infection

Ingestion of infective eggs in contaminated foods

Clinical features

Lofflers syndrome Digestive disorders Urticaria Eosinophilia Intestinal obstruction Bile duct obstruction from heavy infestation

Management

Mebendazole (500mg stat 2nd to 3rd trimester)

STORCH-5

Syphilis Toxoplasmosis Others:

Bacterial vaginosis Trichomoniasis Group B Strep. Listeria E. coli Varicella

Rubella Cytomegalovirus H5:

HIV Herpes Hepatitis B HPV Human Parvovirus

Syphilis
INTRODUCTION Syphilis is caused by Treponema pallidum It is a spirochete: Gram negative with a long slender, helically coiled body. The spirals are so thin that only immunofluorescent staining and dark field microscopy identifies them. T. pallidum has never been cultured continuously on artificial media, in fertile egg or tissue culture. T. pallidum is microaerophilic (survives best at 1-4% O Drying kills spirochetes; Temp. 42C kills them. Penicillin is treponemicidal in minute concentrations but at a slower rate because T. pallidum divides slowly (30 hours)

Pathogenesis, Pathology and Clinical Presentation

Transmission is usually by sexual intercourse. Primary infection is on the skin or mucous membrane of the genitalia In 10-20% , rectal or oral mucosa or perianal skin may be the site of primary infection The organism may penetrate through intact skin or enter through a break in the epidermis The disease may go through stages of primary , secondary ,latent and tertiary syphilis Both primary and secondary syphilitic lesions are rich in spirochetes and highly infectious. Contagious lesions may recur within 3-5 years after infection, but thereafter the individual is non-infectious. Note that the course of syphilis is not affected by pregnancy and the risk of fetal infection (congenital syphilis) is 60% in 1 and 2 syphilis.

Primary Syphilis

Local multiplication at site of entry and spread to nearby lymph nodes and in blood stream occur 210 weeks after infection. The primary lesion is a papule which develops at the site of entry and breaks down to form an ulcer with a clean, hard base. (Hard chancre). The chancre is painless with lymphocytes and plasma cells predominating in the inflammation. The primary lesion always heals spontaneously.

Secondary Syphilis

This occurs 6 weeks - 6 months after the primary lesion. Red maculopapular rash may occur anywhere in the body (may include hands and feet). Moist pale papules (Condylomata lata):Flat topped papules occurring in groups covered by necrotic layer of epithelium and which secrete seropurulent fluid. Sites for the condylomata lata include anus, axillae, mouth and in general wherever contiguous folds of skin produce heat and moisture.

Other Conditions in Secondary Syphilis Syphilitic meningitis Chorioretinitis Hepatitis Nephritis-immune complex type Periostitis

Secondary lesions also resolve spontaneously.

Latent Syphilis

This occurs in 1/3 of untreated cases. Serologic tests remain positive but patient is asymptomatic. The latent phase may last 2-20 years

Tertiary Syphilis

The infection may remain sub-clinical and patient may pass through the primary and secondary stages with no symptoms and yet develop tertiary syphilis 30% of patients achieve complete cure from early syphilitic lesions. 30% of untreated cases remain latent and the remainder may progress to tertiary syphilis.

Lesions of Tertiary Syphilis

Granulomatous lesions: Gummas appear on skin, bones and liver CNS : Degenerative changes

Meningovascular syphilis Paresis Tabes Aortitis, Aortic aneurysm, Aortic valve insufficiency

Cardiovascular

Treponemes are very rare in tertiary syphilis.

Congenital Syphilis

Transplacental transmission to foetus beginning 10-15 weeks of gestation. If the disease is discovered and treated before 18 weeks, the foetus appears to suffer few sequelae. After 18 weeks, signs of congenital syphilis occur in the foetus. Implications a. Intra-uterine foetal death B. Miscarriage C. Still births

Signs of Congenital syphilis in Live-born Babies: Interstitial keratitis Hutchinsons teeth(notched and narrower incisal edge) and Mulberry molar( with alternating nonanatomical depressions and rounded enamel nodules on its crown surface) Saddle nose: Markedly depressed nasal bridge. Periostitis CNS abnormalities : May include 8th cranial nerve hearing loss.

Diagnosis

Darkfield microscopy Immunoflourescence staining A) Non-treponemal antibodies VDRL: RPR TRUST: Toluidine red unhealed serum test VDRL/RPR become positive 2-3 weeks after infection

VDRL/RPR become negative 6 months following treatment. False positive may occur in malaria, leprosy, measles, infectious mononucleosis, SLE, polyathritis nodosa. 1 syphilis-serology is negative and dark field microscopy is positive 2 syphilis both serology and Darkfield microscopy are positive. 3 syphilis serology is positive but darkfield microscopy is negative. TREPONEMAL ANTIBODIES FTA (Fluorescent Trepanoma Antibody) TPHA (Treponema Pallidum Haemagglutination Assay) Treponema pallidum particle agglutination test ( TPPA) Microhaemagglutination for T. pallidum (MHTP)

Treatment

Penicillin is the drug of choice Benzathine Penicillin 2.4 MU, IM as a single dose for primary and secondary and latent syphilis If infection over 1 year give three doses at weekly interval Erythromycin 500mg qid for 14 days may be used in penicillin allergy Procaine penicillin 1.2 MU daily by IM for 12 days and for 21 days in tertiary syphilis may also be used. Typical Jarisch-Herxheimer reaction within 12-24 hours of treatment may occur due to the release of pro-inflammatory cytokines in response to dying organisms. This may occur as fever or a rise in symptoms

Delivery

If no indication for a caesarean section then vaginal delivery is indicated.

Control Prompt treatment of cases Follow up on source of infection and sexual contacts ABC of STI control Maternal screening(VDRL)

HUMAN CYTOMEGALOVIRUS

Human Cytomegalovirus (CMV), is DNA herpesvirus also known as Human Herpes Virus 5 HCMV is one of the TORCH infections that lead to congenital abnormalities It has the ability with other Herpes viruses to establish latency

The incidence of infection in Pregnancy is not known precisely but it is estimated to be 1 in 200 pregnancies, of which 40% will result in fetal Infection Incidence is higher in women who are of low socioeconomic status or who have poor personal hygiene.

CMV resides in the respiratory tracts Genitourinary tracts CMV may be shed in bodily fluids (urine, saliva, blood, tears, semen, and breast milk)

Mode of transmission is thus through; Blood Transfusion Transplantation of Organs Close contacts: Kissing and Sexual Contact Acquired In utero Breastfeeding

What are the symptoms of CMV?

Most children and adults who are infected with CMV do not develop symptoms, whereas others may experience an infectious mononucleosis-like symptoms, three to twelve weeks after exposure: Fever Swollen glands

Classification

Primary Infection Secondary Infection

Primary Infection

Primary Infection is CMV infection in a previously seronegative person. The virus becomes dormant and exists in a latent state, from which it can be reactivated. Its reactivation is designated as SECONDARY INFECTION. (ie. in immunosuppressed state)

However, there are several strains of CMV that infect humans, so reinfection can occur, even in immunocompetent individuals.

Secondary Infection

Secondary Infection is defined as intermittent excretion of the virus, due to either reactivation of an endogenous virus or exposure to a new virus strain from an exogenous source.

Effects of Infection in Pregnancy

Congenital Cytomegalovirus Infection Spontaneous Abortion

Congenital Cytomegalovirus Infection

This is the in utero infection of the fetus with the Human Cytomegalovirus Congenital infections are the result of transplacental transmission of CMV.

Transmission to the fetus may occur because of primary or secondary maternal infection.

The probability of intrauterine transmission following primary infection during pregnancy is 30% to 40%, compared with only 1% following secondary infection. 10-15% percent of congenitally infected infants will have symptoms at birth including ;

intrauterine growth restriction, microcephaly, hepatosplenomegaly, petechiae, jaundice, chorioretinitis, thrombocytopenia, anemia

20% to 30% of them will die, mostly of disseminated intravascular coagulation, hepatic dysfunction, bacterial superinfection Most of the congenitally infected infants (8590%) have no signs or symptoms at birth.

5% to 15% of them will develop sequelae such as sensorineural hearing loss, delay of psychomotor development visual impairment.

Prenatal Diagnosis
The first step in the prenatal diagnosis of congenital CMV infection is; Determination of maternal primary and secondary infection by serological testing. In women with proven CMV infection, the second step is ; To identify fetal infection

Fetal Infection is determined by; non-invasive investigations (ultrasound examination) Invasive procedure (amniocentesis)

Determination of maternal primary and secondary infection by serological testing

The diagnosis of primary CMV infection is ascertained when seroconversion is documented

Seroconversion is the de novo appearance of virus-specific IgG in the serum of a pregnant woman who was previously seronegative.

Serologic diagnosis of primary CMV infection during pregnancy is documented by either seroconversion (the appearance of CMV-specific IgG antibody in a previously seronegative woman) or detection of specific IgM antibody associated with low IgG avidity.

Since intrauterine transmission of the virus occurs in only 30% to 40% of pregnancies in women with primary infection and at a significantly lower rate in women with secondary infection, it is important in cases of proven maternal infection to find out if the fetus is infected.

CMV isolation from amniotic fluid has been recognized as the gold standard for prenatal diagnosis of fetal CMV infection. To achieve the highest sensitivity, the amniocentesis should be performed until at least 7 weeks after the onset of maternal infection and after 21 weeks of gestation because a detectable quantity of the virus is not secreted to the amniotic fluid until 5 to 7 weeks after fetal infection and replication of the virus in the kidney

DIAGNOSIS OF FETAL INFECTION

Ultrasonographic findings are helpful but not diagnostic because CMV has features in common with other intrauterine infections and with other fetal diseases. Moreover, these abnormalities are observed in less than 25% of infected fetuses.

The most frequently reported sonographic findings of fetal CMV infection include: fetal growth restriction, cerebral ventriculomegaly, ascites, intracranial calcifications, abnormality of amniotic fluid volume (usually oligohydramnios), microcephaly, Hyperechogenic bowel, hydrops fetalis, pleural effusion, and Liver calcifications

TREATMENT
Despite advances in the diagnosis of fetal CMV infection, there is no effective therapy. There are no treatments for prenatal or postnatal therapy of the infection.

Vaccines for treatment are still in the research and developmental stages.

How can CMV be prevented?

Transmission of cytomegalovirus is often preventable because it is most often transmitted through infected bodily fluids that come in contact with hands and then are absorbed through the nose or mouth of a susceptible person. People who interact with children should use safe hygiene practices including good hand washing and wearing gloves when changing diapers. Hand washing with soap and water is effective in preventing the spread of CMV

If you develop a mononucleosis-like illness, you should be checked for CMV infection Refrain from sharing food, eating utensils and drinking utensils with anyone. Your doctor can test the CMV antibodies to determine if you have already had CMV infection.

Pregnant women who are infected with CMV rarely have symptoms, but rather their developing baby may be at risk for Congenital CMV Infection and its associted problems to the new born

Bacterial vaginosis

Bacterial vaginosis is the commonest cause of abnormal vaginal discharge in women of reproductive age. It is characterised by an increase in the concentration of anaerobic organisms in the vagina accompanied by a rise in vaginal PH to b/n 4.5-7.0 Organisms often associated with BV are Gardnerella vaginalis, Bacteroides spp , Mobiluncus spp and Mycoplasma hominis

TOXOPLASMOSIS AND PREGNANCY

Toxoplasmosis

is the disease syndrome caused by a protozoan organism called Toxoplasma gondii. It affects most animals most notably sheep, cats, and humans. However the primary host is the felid (cat) family

Epidemiology
Evidence of prior infection with T. gondii is common throughout the world. In the United States, the overall age-adjusted seroprevalence is 22.5%,2 and 15% among women of childbearing age (15 to 44 years). There are approximately 225,000 cases of T. gondii infection per year,

Mode of transmission
Transmission

is a. by eating raw or undercooked infected meat, b. by ingestion of feces of a cat that has itself recently been infected, or c. by transmission from mother to fetus transplacentally. Although cats are often blamed for spreading toxoplasmosis, contact with raw meat is a

What are the risk of getting Toxoplasmosis

Toxoplasmosis rarely causes any symptoms in otherwise healthy adults. However, those with a weakened immune system, such as pregnant women,and AIDS patients may become seriously ill, and it can occasionally be fatal. Primary infection in pregnant women can be transmitted transplacentally to the fetus. Transmission of Toxoplasma to a fetus is extraordinarily rare in

immunocompetent mothers who have had toxoplasmosis earlier in life. ie

Past infection confers resistance to reinfection..

And most new infections in pregnancy are due to reactivation of a prior infection.

The fetus risk of becoming infected rises as your pregnancy progresses. pregnant woman get infected with toxoplasmosis in the first trimester, the risk that the fetus will also be infected is about 15 percent. pregnant woman get infected in the second trimester, the

If

If

fetus risk is about 30 percent, and

in

the third trimester ,it's 60 percent.

NOTE: Although the transmission rate is higher in late

pregnancy, the severity of congenital toxoplasmosis is highest if the fetus becomes infected in the first trimester.

Symptoms and signs in a pregnant woman

Pregnant women infected with T. gondii generally do not have clinical manifestations, although some may have a mild mononucleosis-like syndrome o fever, oMuscle stiffness, ojoint pain, oFatigue regional lymphadenopathy, Hepatomegaly and slenomegaly OR occasionally chorioretinitis.

These symptoms may be so mild as to go unnoticed. Illness lasts 1 to 12 weeks and is

often dismissed as
a bad cold or mononucleosis.

Symptoms and signs in the neonate ( Congenital Toxoplasmosis )

Most

neonates are asymptomatic at birth on routine pediatric examination. Clinical manifestations of toxoplasmosis in fetuses and neonates vary. The classic triad of findings consists of chorioretinitis, hydrocephalus, and intracranial calcifications However this typical triad of signs does not always occur.

Other signs suggestive of Toxoplasmosis in the neonate

fever microcephaly, seizures Prematurity Intrauterine growth restriction (small-for-gestational-age ) Jaundice Hepatosplenomegaly Myocarditis Pneumonitis Thrombocytopenia Various rashes Neurologic involvement which includes chorioretinitis, hydrocephalus, intracranial calcifications, microcephaly and seizures often prominent .

 Nevertheless,

Deafness, mental retardation, and learning difficulties are often detected only later in life.

Investigations
Serial IgG measurement (for maternal infection) Amniotic fluid PCR (for fetal infection) Serologic testing, brain imaging, CSF analysis, and ophthalmologic evaluation (for neonatal infection)

The most reliable Serologic testing are the Sabin-Feldman dye test, the indirect immunofluorescent antibody (IFA) test, and the direct agglutination assay

Management
Sometimes

spiramycin for pregnant women , sulfadiazine , and leucovorin

Pyrimethamine

for neonates

Prevention
1.

2.

3.

4.

Probably the most important thing is to be careful when cooking raw meat, especially lamb and pork. A PREGNANT WOMAN NOT EAT MEAT OR TASTE MEAT BEFORE IT IS FINISHED COOKING. Avoid handling cat or changing cat litter if possible. If she must do it, she must wear gloves and wash her hands thoroughly afterward. Wearing gloves during any contact with soil or sand because it might contain cat feces. Wash hands thoroughly after coming in contact with soil or sand. Cook foods at safe temperatures and use a food thermometer to ensure that meat is cooked thoroughly. The meat should not look pink and the juices should be clear.

Preventioncontinue
5. A pregnant woman should not drink raw milk, especially goats milk 6. Peel or thoroughly wash fruits and vegetables before eating.

7. Wash cutting boards, dishes, counters, utensils and hands with hot, soapy water after they have come in contact with raw foods.

Risk factors
Women with IUCD Women of afro-caribbean descent Pregnancy Frequent douching Multiple sexual partners Frequent use of antibiotics Women who undergo termination of pregnancy Sexually active women b/n 15 and 44 years

pathophysiology

BV arises from chemical and biological imbalances that disrupts the normal vaginal flora, allowing anaerobes which are in lower concentrations to over-grow whiles reducing the amounts of lactobacillus in the vagina

Symptoms

The principal symptom of bacterial vaginosis is fishy smelling discharge. It is characteristically thin, homogeneous and adherent to the walls of the vagina and may be white or yellow in colour. The smell is particularly noticeable around the time of menstruation or following intercourse

Effect of BV on pregnancy
MATERNAL EFFECTS Second trimester abortions Infection of foetal membranes Preterm premature rupture of membranes Preterm delivery Puerperal sepsis FETAL COMPLICATIONS Still birth IUGR Low birth weight Neonatal sepsis

Effects of pregnancy on BV
Not much is known about the effects of pregnancy on BV but it is believed that increase in levels of stress hormone (cortisol) during pregnancy with resultant fall in immunity may account for the increase in cases of BV in pregnancy

Diagnosis
Diagnosis is made in the clinical setting using the composite(Amsel) criteria. 1)Vaginal PH>4.5 2)Release of a fishy smell on addition of alkali(10% KOH). Positive amine(whiff) test 3)A characteristic discharge on examination 4)Presence of clue cells on microscopy

NB. At least 3 of the four conditions must be present to make a diagnosis of BV

Management
a)PREVENTION Prevention is aimed at avoiding any activity that has the tendency to disrupt the normal vaginal flora and these include 1)Avoiding douching 2)Avoiding prolonged and repetitive use of antibiotics 3)Good sexual practices 4) Good hygienic practices especially in the area around the genitals

Management 2
B) TREATMENT This involves the use of antibiotics and the one commonly used is metronidazole. Regimen: 500mg bd for 7 days NB clindamycin can also be used

Complications of BV
May predispose to other forms of vaginal infections and STIs eg herpes and gonorrhea. May cause second trimester abortions May lead to preterm labour May lead to infected surgical scars

TRICHOMONIASIS IN PREGNANCY

Trichomoniasis, commonly known as trich is a sexually transmitted disease that is caused by a microscopic parasite, Trichomonas vaginalis

How does it present?

Asymptomatic Yellowish or greenish vaginal discharge with a frothy appearance and an unpleasant odour. Vulva irritations and itch Discomfort on urination or intercourse Less commonly lower abdominal discomfort.

Symptoms may appear soon after the infection is contracted or later so the appearance of symptoms does not necessarily mean that the infection was acquired recently.

Effects of trichomoniasis on pregnancy

Preterm birth Preterm premature rapture of membranes(PPROM) Low birth weight It also increases susceptibility to HIV infection if the woman is exposed to it. There could also be a possible infection of the baby during delivery.

Investigations
The specimen taken is a high vaginal swab for microscopy and culture. Microscopy; the vaginal secretion is mixed with saline and viewed under the microscope. It shows numerous polymorphonuclear cells and motile organisms with 4 moving flagellaethe trichomonads.(has 50-60% sensitivity) Culture; the vaginal secretion can be cultured using the Fineberg-Whittington medium.

treatment

It is treated with a course of oral metronidazole, The partner should be treated as well whether he is showing symptoms or not. They are to abstain from sex until they have finished the treatment and are symptom-free.

Prevention

Having one faithful sexual partner Protection using condoms during sexual intercourse

RUBELLA

AETIOLOGY A disease caused by rubella virus. In the adult it is usually a mild febrile illness with a faint rash. Rubella is important because of the damage it can cause to the foetus when a mother contracts the infection during pregnancy. Incubation period is from 14-23 days Period of infectivity is from a week to 5days after the appearance of the rash. Mode of transmission is through respiratory droplets and contacts. Infection of women in the first 12weeks of pregnancy carries a very high risk(95%) of fetal infection. In 20% of these serious damage to the fetus occurs.

CLINICAL FEATURES
In the adult; Mild fever Sore throat Enlarged tender lymph nodes (occipital ,retro auricular, posterior cervical.

In the baby; Immediately after birth;

Greggs triad-Cataract, Congenital heart disease and deafness.

First week of life; Hepatosplenomegaly, Jaundice, Hypertonia, Lethargy, Convulsions, Cloudiness of cornea, Microophthalmia, Respiratory distress, LBW, Purpura

DIAGNOSIS

Rubella should be suspected in any SGA baby born with congenital anomalies Congenital rubella can be diagnosed by detecting the virus in secretions from the throat, urine, stool, CSF, blood, eyes, ears. Maternal diagnosis is based on serology A high IgG Ab titre is suggestive of recent infection

PREVENTION
There is no specific treatment available so prevention is the key. *Vaccination with MMR between 9 and 12 months of life. *Non immune women are advised to stay away from known cases of rubella. *Encouragement of natural infection early in female children

PARVOVIRUS B19

CHARACTERISTICS Non-enveloped virus with icosahedral symmetry and single stranded linear DNA genome. Virion contains no polymerase. There is one serotype. TRANSMISSION Respiratory secretions, droplets and transplacental. DISEASES Slapped cheek syndrome ( erythema infectiosum), aplastic anemia, hydrops fetalis ( from maternal infection ) with risk of fetal loss of 10% in infection before 20 weeks.

PATHOGENESIS
1. 2.

The virus induces immune complex formation that deposit in joints and the skin, causing erythema infectiosum. Virus preferentially infects erythroblasts, causing aplastic anemia in patients especially those with hereditary anemias. The virus can infect the fetus and cause severe anemia, leading to congestive heart failure and edema ( hydrops fetalis ). DIAGNOSIS Clinical, by characteristic rash and Serology.

TREATMENT No specific antiviral therapy. Supportive. IV gamma globulin may be given to women in aplastic crises with viraemia. PREVENTION There is no drug or vaccine.

HEPATITIS B & PREGNANCY

Hepatitis B

Hepatitis B is an infectious illness caused by hepatitis B virus (HBV) which infects the liver of hominoidea, including humans, and causes an inflammation called hepatitis.

Hepatitis B

About a third of the world's population, more than 2 billion people, have been infected with the hepatitis B virus. This includes 350 million chronic carriers of the virus.

Hepatitis B modes of transmission

Infected body fluids

Blood > semen or vaginal mucus > saliva, tears, breast milk No virus in urine, faeces, or sweat

Sexual (30% of sexual partners infected) Perinatal (neonatal contact with mothers blood at
delivery)

Needlestick (= very high risk; much greater than HIV) Blood transfusion (mostly historical)

Signs and symptoms: Acute Infection

Acute infection with hepatitis B virus is associated with acute viral hepatitis an illness that begins with

general ill-health loss of appetite nausea vomiting body aches mild fever dark urine and then progresses to development of jaundice

Signs and symptoms: Acute Infection

The illness lasts for a few weeks and then gradually improves in most affected people. A few patients may have more severe liver disease (fulminant hepatic failure), and may die as a result of it. The infection may be entirely asymptomatic and may go unrecognized.

Signs and symptoms: Chronic Infection

Chronic infection with hepatitis B virus may be either asymptomatic or may be associated with a chronic inflammation of the liver (chronic hepatitis), leading to cirrhosis over a period of several years. This type of infection dramatically increases the incidence of hepatocellular carcinoma (liver cancer)

Natural course of Hepatitis B

Infectious contact
~12 weeks <1% fulminant hepatitis

(35%)

Transient, asymptomatic infection

(65%)

Acute hepatitis
(5% of adults; 90-95% of neonates)

Complete recovery
(95% of adults; 5-10% of neonates)

Chronic infection
(20%)

Asymptomatic carriers
(80%)

Cirrhosis or cancer

~1% of all infected people

Effects During Pregnancy

When a pregnant woman is infected with hepatitis B virus, there is a chance she will infect her fetus. Whether the baby will get the virus depends on when infection occurred. If it was early in pregnancy(1ST trimester ), the chances are less than 10% that the baby will get the virus. If it was late in pregnancy (3RD trimester), there is up to a 90% chance that the baby will be infected.

Effects During Pregnancy

HBV infection does not appear to cause birth defects, but there appears to be a higher incidence of low birth weight among infants born to mothers with acute infection during pregnancy In one small study,acute maternal hepatitis (type B or nontype B) had no effect on the incidence of congenital malformations, stillbirths, abortions, or intrauterine malnutrition. However, acute hepatitis did increase the incidence of prematurity

Effects During Pregnancy

Hepatitis can be severe in babies. It can threaten their lives. Even babies who appear well may be at risk for serious health problems.

Infected newborns have a high risk (up to 90%) of becoming carriers. They, too, can pass the virus to others when they become adults.

Effect of Pregnancy on Hepatitis B

In general, women with chronic hepatitis B do well during pregnancy. However, pregnancy is associated with high levels of adrenal corticosteroids, which is postulated to increase levels of viraemia.

It has been known for some time that a proportion of women have hepatitis flares with or without HBeAg seroconversion within the first months after delivery. Seroconversion rates of 12.5% to 17% have been described.

Effect of Pregnancy on Hepatitis B

Also, cases of exacerbation of hepatitis and even fulminant hepatic failure have been described in the peripartum period. It therefore appears prudent to monitor HBVinfected women closely for several months after delivery for hepatitis flares and seroconversion.

Hepatitis B- Diagnosis

The tests, called assays, for detection of hepatitis B virus infection involve serum or blood tests that detect either viral antigens (proteins produced by the virus) or antibodies produced by the host.

The hepatitis B surface antigen (HBsAg) is most frequently used to screen for the presence of this infection.

It is the first detectable viral antigen to appear during infection. However, early in an infection, this antigen may not be present and it may be undetectable later in the infection as it is being cleared by the host

Prevention
Hepatitis B is transmitted through body fluids; prevention is thus through the avoidance of such transmission:

unprotected sexual contact blood transfusions re-use of contaminated needles and syringes vertical transmission during child birth

Hepatitis B Drug Treatment

Available Drugs :

Interferon a (must be given by injection) HBV polymerase (RT) inhibitors (originally for HIV)

lamivudine adefovir entecavir telbivudine tenofovir

Drug resistance is common Drug combinations

Hepatitis B Immunization

Passive

HB immune globulin (HBIG) effective in emergencies (e.g., needlestick) Expensive recombinant HBV vaccine (HBsAg) 3 doses (0, 1 mo., 6 mos.) revaccination not necessary

Active

Candidates:

infants born to HBsAg+ mothers (+HBIG) people with occupational risk all sexually active people sexual partners of carriers

TREATMENT DURING PREGNANCY

Pregnancy is not a contraindication to vaccination. The use of active and passive immunoprophylaxis to reduce the risk of perinatal transmission of HBV is well accepted in clinical practice. HBIg given at the time of birth in combination with three doses of the recombinant hepatitis B vaccine given over the first 6 months of life has been up to 95% effective in preventing perinatal transmission

TREATMENT DURING PREGNANCY

Viable treatment choices are limited to lamivudine, tenofovir, and telbivudine. Of these, lamivudine and tenofovir appear to be the therapeutic options with reasonable human exposure and safety data in pregnancy.

Pregnant Hepatitis B carriers should be advised to

Abstain form alcohol use

Avoid hepatotoxic drugs such as acetaminophen (Tylenol) that may worsen liver damage.

Not donate blood and body organs

Not share any personal items that may have blood on them (e.g., toothbrushes and razors). Inform the infants pediatrician, OB/GYN, and labour staff that they are hepatitis B carriers.

Pregnant Hepatitis B carriers should be advised to

Make sure their baby receives hepatitis B vaccine at birth, one month, and six months of age as well as H-BIG at birth. Be seen at least annualy by their regular Medical Doctor. Discuss the risk for transmission with their partner and discuss the need for counseling and testing

Breast feeding

With appropriate hepatitis B immunoprophylaxis, breast-feeding poses no additional risk for transmission from infected hepatitis B virus carriers.