Contact-transmitted infections

CONTACT –
TRANSMITTED
INFECTIONS
Dr. Dalia El-Shafei
Assist.Prof., Community Medicine Department, Zagazig University
http://www.slideshare.net/daliaelshafei

 Invasion of the skin or mucous membranes by a pathogenic
organism or parasite.
 Infection in which entrance of the pathogenic organism (or the
parasite) occurs through the skin or mucus membranes.
 Some infectious agents can invade the intact (undamaged)
skin or mucous membranes, but the majority needs injured
surfaces in the form of abrasions, scratches, wounds or ulcers.

Viral
AIDS
Hepatitis “B&C”
Rabies
Bacterial
Anthrax
Gas gangrene
Gonorrhea
Leprosy
Tetanus
Parasitic
Ancylostomiasis
Schistosomiasis
Spirochetes
Syphilis

VIRAL DISEASES TRANSMITTED BY
CONTACT

HBV, HCV and HDV are transmitted mainly percutaneous “contact infections”.
HAV is transmitted mainly by faeco-oral transmission )food borne disease(.
HDV & HFV are similar to HBV.
HEV is similar to HAV.
HGV is similar to HCV.
Other viruses cause acute hepatitis e.g. cytomegalovirus, Epstein-Barr virus.

EPIDEMIOLOGY OF VIRAL HEPATITIS
• Usually the disease is self-limited, however some cases show
massive or chronic hepatic necrosis & chronic hepatitis.
• Virus B and C may be complicated by liver cirrhosis &
hepatocellular carcinoma.
• An estimated 248 million people have chronic HBV infection
globally. In Egypt the prevalence is < 2%.

Viral hepatitis C is a major health problem in Egypt.

• Egypt is one of the countries most affected by HCV.
• The Egypt Demographic and Health Surveys (EDHS) measured antibody
prevalence among the adult population aged 15–59 years at 14.7% in 2009
& at 10.0% in 2015 substantially higher than global levels.
• Egypt developed a national strategy for HCV control & established HCV
prevention & treatment programs.
• Following successful negotiations for 99% discounted direct-acting antivirals
(DAAs) prices, Egypt launched an ambitious national HCV treatment program
aiming to treat over 250,000 chronically infected individuals per year, with the
goal of achieving a national chronic infection prevalence of < 2% by 2025.
• Despite this progress, existing evidence suggests ongoing HCV transmission in
Egypt, with higher incidence levels relative to other countries.

Hepatitis B Hepatitis C
CausativeAgent
• Hepatitis B Virus (HBV)
• DNA virus
• Contains: HBsAg, HBcAg,
HBeAg
• It is more resistant than virus
A to heat & disinfectants and
can retain infectivity for at
least 1 month at room
temperature.
• Hepatitis C Virus (HCV).
• RNA virus,
• There are 6 known genotypes and 50 or
more subtypes of HCV
• Types 1,2 and 3 are worldwide while
type 4 is found in North Africa and
Middle East, type 5 in south Africa, 6 in
Asia
• About 90% of HCV in Egypt belongs to
subtype 4b which has less response to
interferon therapy.

HCVHBV
Cases, carriersCases, carriersReservoir
1-2 w before symptoms, clinical
course
So long is HBs AG (+ve) appear
30-60 days after infection
Period of
communicability
1- Percutaneous exposure to infective body fluid
2-Insufficient sterilized needles, syringes, razors, toothbrushes,
surgical & dental instruments, blood transfusion (Blood borne
pathogens “BBP”).
3- Maternal fetal transmission
4- Organ transplantation
5- Sexual transmission
Mode of
transmission

HCVHBV
2-12 weeks (average 6 weeks)60-150 days (average 90 days)IP
1-Asymptomatic or mild symptoms.
2.Low grade fever, fatigue, N,V , Rt. sided
abdominal pain,
3.Jaundice.
4.Self-limiting infection after 3-6 months.
No jaundice.
5.Chronic infection “80%”: weakness,
pain in Rt. upper abdomen.
1-Nonspecific prodroma of
malaise, fever, headache,
myalgia.
2- Dark urine, jaundice.
3-Asymptomatic or have illness
not specific for hepatitis B
“50%”.
C/P
Liver cirrhosis “25%”, liver failure, Cancer
liver, Renal disorders, formation of auto-
antibodies, DM
Fulminant hepatitis, Chronic
hepatitis, Liver cirrhosis, Causes
up to 80% of hepatocellular
carcinoma.
Complications

HCVHBV
-C/P: ↑ liver enzymes- detection of AB by
ELISA
+VE ELISA: PCR test
-Liver biopsy
- Genotyping of HCV
-Serum fibrosis markers
C/P- ↑ liver enzymes- markers:
HBsAb: active or past infection
HBsAg: disease or chronic carrier
state-
HBcAB:recent infection
Diagnosis

HCVHBV
No specific preventive measures1- HBV, 3 Doses,0.5 ml each at 0, 1,6 months (for who?).
Give 95% protection for 7 years.
2- Ig, 0.1ml/kg, 2 doses 1 month apart given at once after
exposure (for who?) not > 48hs
3- Combined vaccine+ Ig
1ry
(specific)
Prevention
1- Screening & testing blood, plasma and organ tissue donors.
2- Health education.
3- Sterilization of surgical instruments & use of disposable syringes.
4- Prevention of drug abuse & needle shared injections.
5- Prevention of tattooing, prevention of use of common razors or scissors.
6- Surgeons should use thick protective gloves.
7- Proper handling & disposal of sharp instruments and needles.
8- Quarantine measures: some countries prevent HCV patients from entrance.
1ry
(general)
Cases: case finding- notification-isolation-disinfection-HE-treatment (antiviral, antioxidants).
Contact: enlistment- examination-HE-specific protection in case of HBV (vaccination,
seroprophylaxis)
2ry
Rehabilitation of liver failure or cancer liver cases.
3ry

TREATMENT
• HCV TTT continues to evolve rapidly.
• Since 2014, several new all-oral direct-acting
antiviral agents have been approved for use.
• Egyptian MOH proposed a new national
strategy to control the HCV epidemic with a
greater capital fund & with support from the
WHO as well as other institutes.
• This scheme was entitled “The Plan of Action
for the Prevention, Care and Treatment of
Viral Hepatitis 2014–2018” & promoted
sofosbuvir (Sovaldi™) as its 1ry ttt.

The scheme aims to treat 300,000 patients annually
MOH
38%
HIO
51%
Private
payments
3% Patients
8%
TTT Cost

REMMEBER
Risk of infection & required post exposure prophylaxis for the
3 most commonly transmitted pathogens

Definition: acute viral zoonosis, transmitted to man by bite of an
infected animal & causing acute encephalomyelitis illness.
Causative organism: Rabies virus, RNA rhabdovirus with 5
genetically related viruses.

Reservoir: Domestic & wild animals “dog, cat, fox, wolf, rats,
bat, etc”.
Exit: in saliva of rabid animals.
Modes of transmission: Infection is transmitted with saliva
through the bite of an infected animal usually or when saliva gets
on an injured skin by lick. No man to man infection.

IP:
- Depends on the distance
between the site of bite & brain.
- Usually 2-8 weeks, but up to 1
year.
PATHWAY OF
RABIES VIRUS

Clinical picture:
History of animal
bite.
Non-specific
manifestation:
e.g. FHMA.
Specific
manifestations:
Paraesthesia
Aerophobia
Hydrophobia
Difficult
swallowing
Convulsions
Death:
1-2 weeks
Convulsions
Respiratory
paralysis

Diagnosis
C/P following
a history of
an animal
bite.
Detection of
virus particles
in saliva,
C.S.F or urine
Detection of
viral antigen
in skin biopsy
using direct
fluorescent
antibody
technique.
Rising
antibody
titers in blood
or C.S.F.

Control:
Measures for animals:
Destruction of stray
dogs.
Vaccination of domestic
animals: inactivated
rabies vaccine every 2
years & giving license.
Quarantine of imported
animals

MEASURES FOR MAN
(A) Pre-exposure vaccination: vaccination of at risk e.g. night guards
& zoo workers. 3 inactivated types of rabies vaccines are used:
I.M., 3 doses, 1 ml each, in deltoid region on days 0, 7, and 21 or 28.
Booster dose every 2 years if risk of exposure continues.
Human diploid cell
vaccine (HDCV)
Rabies vaccine
adsorbed (RVA)
Duck embryo vaccine
(DEV)

MEASURES TO THE WOUND (BITE)
• Immediate local ttt of animal bite & scratches through repeated flushing &
cleaning of wound with soap & water.
• A rabies immunoglobulin (20 IU/kg) or antiserum (40 IU/kg) is infiltrated
locally around the wound (half the dose). The other half is given I.M.
• Wound should not be sutured then wound is dressed.
• Give tetanus prophylaxis & antibacterial treatment.

Measures for
cases
Notification to LHO.
Isolation.
Disinfection of saliva &
soiled articles.
Treatment: only
symptomatic
Measures of
contacts:
No specific measures, as
there is no man to man
transmission; however,
avoid contamination of
skin wound or mucous
membrane by patient's
saliva.

A life threatening clinical condition that represent the late clinical
stage of infection with HIV which results in progressive damage
to the immune and other organ systems specially CNS.
Acquired Immunodeficiency Syndrome (AIDS)
Causative agent:
 Human immune deficiency virus (HIV): DNA retrovirus.
 2 serologically & geographically distinct types with similar
epidemiological characteristics:HIV-1 & HIV-2.

Specific affinity to T-helper lymphocyte cells causing
their depletion.

 Reservoir: man
 Exit: in blood and body fluids e.g. semen, vaginal secretion,
saliva and tears.
 Period of communicability: so long the infected person is alive.
 IP: variable, but 50% of those infected develop AIDS about 10
years after infection.

Specific indicator diseases:
Opportunistic
infections
• Pneumocystis
carinii
pneumonia
• Chronic
cryptosporidiosis
• CNS
toxoplasmosis.
Neurologic
diseases
• Dementia
• Sensory
neuropathy.
Cancers
• Kaposi sarcoma
• Hodgkin's
lymphoma.
Others
• T.B.

HIV CONTROL
Preventive measures:
1ry (HE - ↑ religious roots - disposable syringe -
testing blood donors - no tattooing or acupuncture)
2ry
Measures for cases: Case finding – Notification - Isolation is
unnecessary - Disinfection - ttt of opportunistic infections,
Antiretroviral ttt.
Measures for contacts: Notification – Screening – HE - No vaccination
or chemoprophylaxis).

No vaccination is available yet.
Pre-exposure prophylaxis (PrEP)
• Highly effective in preventing HIV
infection.
• 2 oral antiretroviral “ARV”
medications (tenofovir &
emtricitabine)
• Co-formulated as a single pill
(Truvada) that is taken once daily.
Post-exposure prophylaxis (PEP)
• 2014 WHO guidelines
• Irrespective of exposure source
• As soon as possible to be effective
• Within 72 hours (3 days) after a
possible exposure
• 3 or more ARV medicines every day
for 28 days.

N .B.
WHO recommends immunization of asymptomatic HIV infected
children with the EPI (Expanded program Immunization) vaccines;
those who are symptomatic should not receive BCG vaccine.
Live Measles-Mumps-Rubella (MMR) & polio vaccines are
recommended for all HIV-infected

CAUSATIVE AGENT
Clostridium tetani

PERIOD OF COMMUNICABILITY
It is the only vaccine-preventable disease that is infectious
but not contagious from person to person.
IP.: 6-8 days

Mode of
infection
Surgical
(postoperative)
tetanus
Puerperal
tetanus
Contamination
of wounds
Neonatal
tetanus

SYMPTOMS
- Tetanic seizures (painful,
powerful bursts of ms.
contraction)
- Ms. spasms of larynx or
chest wall: asphyxiation
- Stiffness of abdominal &
back ms.: resus sardonicus

The back muscles are more
powerful, thus creating the
arc backward
“Oposthotonus”
Baby has neonatal tetanus
with complete rigidity.

Newborn showing risus sardonicus
& generalized spasticity

TYPES OF TETANUS:
A- MOST COMMON TYPES
Generalized tetanus
- descending pattern: lockjaw  stiffness of neck  difficulty swallowing
 rigidity of abdominal and back muscles.
- Spasms continue for 3-4 weeks, and recovery can last for months
- Death occurs when spasms interfere with respiration.
Neonatal tetanus:
- Form of generalized tetanus that occurs in newborn infants born without
protective passive immunity because the mother is not immune.
- Usually occurs through infection of the unhealed umbilical stump,
particularly when the stump is cut with an unsterile instrument.

B-Uncommon types:
• Local tetanus: persistent muscle contractions in the same
anatomic area as the injury, which will however subside after
many weeks; very rarely fatal; milder than generalized tetanus,
although it could precede it.
• Cephalic tetanus: occurs with ear infections or following
injuries of the head; facial muscles contractions.

DIAGNOSIS OF TEATANUS
History
C/P
Lab diagnosis:
Difficult

CONTROL OF TEATANUS
Measures
Preventive
General
Special forms
Neonatal
Surgical
Puerperal
Specific measures
Active immunization
Infant
Pregnant
High risk
Injury
Wound
Immunization
Control

GENERAL MEASURES
1.Community development & cleanliness of the environment.
2. Control of animal reservoir e.g. segregation of stables & animal
sheds from residential areas, replacing animal carts with mechanical
vehicles.
3. Health education about the disease & importance of environmental
sanitation.

MEASURES FOR SPECIAL FORMS OF TETANUS
• Aseptic cutting & dressing of the umbilical cord
• Training & health education of birth attendants for sound health behavior.
• Pre-conceptional or prenatal active immunization of mothers in high risk areas.
Neonatal tetanus
• Proper sterilization of catgut & instruments and asepsis in care of surgical wounds.
• Clean hospital environment & surrounding.
Surgical infection
• Active immunization of pregnant in high risk areas.
• Proper asepsis & sterilization in labor or abortion.
• Chemoprophylaxis after labor or abortion.
Puerperal infection

SPECIFIC MEASURES:
A-ACTIVE IMMUNIZATION BY TETANUS TOXOID VACCINE
1. Infants:
DPT compulsory, at 2, 4 & 6 months, 0.5 ml, I.M., then booster dose at 18
months.
DT is used instead of DPT after 4 years.

A-ACTIVE IMMUNIZATION BY TETANUS TOXOID VACCINE
1st
• 1st contact with the health service (in 1st pregnancy).
2nd
• At least 4 weeks after 1st dose.
3rd
• 6-12 months after 2nd dose or during subsequent pregnancy.
4th
• 5 years after 3rd dose or during subsequent pregnancy.
5th
• 10 years after 4th dose or during subsequent pregnancy.
2. Pregnant mothers: to prevent neonatal tetanus. 5 doses of tetanus toxoid:

3 doses are given as
follows
1st dose (0.5ml)
2nd dose (0.5 ml)
3rd dose (1 ml)
3-High risk groups: e.g. Military
forces, soldiers, farmers, night
guards and pregnant.
“Immunity for 10 years, so booster
dose is given every 10 years”.
4 ws
6 months

B-MANAGEMENT OF INJURED PERSONS
Prevent further toxin production by:
Cleaning & local debridement of
the wound by removing foreign matters
& necrotic tissues, then application of
local antiseptic solution.
Suturing & dressing of the wound.
Chemoprophylaxis: Antibiotic (e.g.
penicillin or tetracycline) &
metronidazole.

TetanusImmunization
No record of
immunization or > 10
years
1st dose TT + HIG
2nd dose after 4 ws
3rd dose after 6 months
Within 10 years Booster dose TT

II-CONTROL MEASURES FOR CASES:
Notification to the LHO.
Isolation in a quiet room.
Treatment: Human immunoglobulin (3000-6000 I.U.) or equine antitoxin
(30,000 I.U.) I.M. with precautions for serum reaction.
Surgical care of the wound.
Chemoprophylaxis (e.g. penicillin & metronidazole).
Sedatives to avoid stimuli.
Tracheostomy is performed if needed.
Active immunization should be initiated concurrently with therapy.

NICE TO KNOW
The Maternal and Neonatal Tetanus elimination initiative was
launched by UNICEF, WHO in 1999, revitalizing the goal of MNT
elimination as a public health problem - defined as less than one
case of neonatal tetanus per 1000 live births in every district of
every country

GAS GANGRENE
It is a severe form of wound infection characterized by destruction
of tissues and muscles (with production of gas) and toxaemia.

Causative organisms:
Two groups of anaerobic spore-forming clostridia:
2ry Invaders
Proteolytic & Facilitate growth
of the 1ry organisms.
Cl. histolyticum, Cl.
sporogenes & others.
1ry Organisms
Saccharolytic & Toxigenic.
Cl. welchii, Cl. oedematients,
& Cl. septicum.

Modes of transmission:
Contamination of deep lacerated wounds with spores of causative organisms.
Infection of the uterus following septic abortion.
Postoperative infection may occur due to contamination and deficient sterilization of
skin.

SYMPTOMS
High fever Shock
Massive tissue
destruction
Blackening of
skin
Severe pain
around a skin of
wound
Blisters with gas
bubbles near the
infected area
Tachycardia &
tachypnea
Toxemia &
Death
I/P: 1-7 days

CONTROL OF GAS GANGRENE
Prevention
• Surgical care of injuries, removal of any foreign matter and excision of
damaged tissues.
• Aseptic techniques in surgery and chemoprophylaxis with antibiotics.
• Emergency care of abortion to prevent puerperal infection.
• Sero-prophylaxis by polyvalent antitoxin I.M.
Measures
for cases
• Early diagnosis and surgical management.
• Penicillin in massive doses
• Sero-therapy in proper dose.
• Sterilization of any used object or material.

Source of infectionAgent
- Domestic animals: Cattle, goat, horse, pigs, sheep.
- In blood, hair, stool, meat
- No man to man infection except in pneumonic anthrax
Bacillus anthracis
spore forming bacilli
(zoonotic disease)
IP: 2-7 days
Anthrax
(wool sorter’s disease)
Malignant pustule

Cutaneous: “most common, benign”
pruritic vesicle at contact site as face,
neck. Ulcer, black scar.
Gastrointestinal: GE, intest. oedma,
obstruction, death
Inhalation (pneumonic): “most serious
form” cough, fever, massive oedma of
neck & chest, death within 48hs

Modes of transmission
Cutaneous
anthrax
• Contamination of skin abrasions through contact with diseased animals or
handling infected tissues or organs.
• Using unsterilized shaving brushes made of natural bristles.
Intestinal
anthrax
• Ingestion of contaminated milk or insufficiently cooked meat of diseased
animals.
Pneumonic
anthrax
• Inhalation of spores with dusty air of raw wool during the process of wool
sorting (wool sorter's disease).
• Droplet infection from pneumonic anthrax case to a contact.

Diagnosis
History &
clinical
picture
Gram stained
smears from
skin lesions.
Blood
cultures.

Prevention
Protection of
people at risk
Control of source
of infection
Control
Measures for
cases
Measures for
contacts
Specific prevention

Protection of people at risk
• Health education.
• Disinfection of raw wool & hair.
• Quarantine measures for raw
wool & hair.
• Vaccination with anthrax
vaccine for occupational
exposure.
Control of reservoir (sources) of
infection
• Eradication of anthrax in
animals:
• 1- Sanitary clean environment.
• 2- Veterinary care.
• 3-Vaccination “annual”: all
domestic animals at risk in
endemic areas.
• Control of diseased animals:
• 1- Isolation of diseased animals.
• 2- Disinfection of discharges.
• 3-Carcasses of dead animals:
incinerated or buried in a deep
pit.

• Notification to LHO.
• Isolation at hospital or special place.
• Disinfection of discharges from lesions & soiled articles.
• Chemotherapy: Penicillin. Tetracyclines, Erythromycin
and Chloramphenicol are also effective. The U.S.
military recommends parenteral ciprofloxacin or
doxycycline for inhalation anthrax.
Measures for cases
• Contacts of respiratory cases are isolated for 7 days.
Measures for contacts

Chronic granulomatous disease
Mycobacterium leprae
Primarily affecting skin, mucous
membranes of upper respiratory
tract & peripheral nerves

 Causative agent:
Mycobacterium leprae, acid-fast, gram-positive bacillus.
 Reservoir:
1 - Humans (the main reservoir).
2 - Wild armadillos, mangabey monkeys & Chimpanzee: naturally
infected with M.leprae.

Modes of transmission:
• Humans are the only significant reservoirs.
• The disease is in all likelihood transmitted from the nasal
mucosa of a patient to the skin and respiratory tract of another
person.
Transmission requires close contact.

IP: 9 months to 20 years (average 4-8 years).

Indeterminate leprosy
• Hypo-pigmented maculae with ill-defined borders; if untreated, it may progress
to tuberculoid, borderline or lepromatous disease.
Lepromatous (multibacillary) leprosy
• Symmetrical & bilateral nodules, papules, macules & diffuse infiltrations “numerous &
extensive”.
• Involvement of the nasal mucosa: crusting, obstructed breathing & epistaxis.
• Ocular involvement: iritis & keratitis.
Tuberculoid (paucibacillary) leprosy
• Skin lesions: single or few, sharply demarcated, anesthetic or hypo-anesthetic.
• Bilateral asymmetrical involvement of peripheral nerves tends to be severe.
Borderline leprosy
• Features of both polar forms and is more labile.

DIAGNOSIS OF LEPROSY:
Characteristic skin lesions (↓or lost sensation, thickened peripheral nerves).
Skin smear stained with Ziel-Neelsen stain: most important method.
Nasal scrapping: assessing the infectiousness of a patient.
Nerve biopsy: when there is no skin lesion.
PCR to detect M. leprae DNA.
Lepromin test

Lepromin test
• Not diagnostic test but measures the degree of cell-mediated immunity.
• Used for classification.
• -ve in lepromatous type & strongly +ve in tuberculoid type.
• Useful to assess susceptibility of population in community surveys.

PREVENTIVE MEASURES:
General measures
• Improvement in general hygiene, better
housing & prevent overcrowding.
Specific measures
• BCG immunization gives considerable
reduction in the incidence of
tuberculoid leprosy.

CONTROL MEASURES
Measures for cases
• Case finding e.g. surveys in endemic areas.
• Notification to LHO.
• Isolation: “stigmatization”. No restrictions
in employment or attendance at school are
indicated.
• Disinfection.
• Specific treatment:
• Combined chemotherapy to avoid
resistance.
• Rifampicin 600 mg once monthly +
dapsone 100 mg/ day + clofazimine 50 mg
once a day and 300 mg once a month.
• Minimum duration of ttt is 12 months or
moreuntil skin smears are negative.
• Release: after becoming bacteriological
free.
• Enlistment
• Initial examination then periodically at 12
months intervals for at least 5 years after
last contact with an infectious case.
• Chemoprophylaxis with dapsone is not
recommended because of limited
effectiveness and danger of resistance.

A parasitic disease caused by a trematode infecting
venous system & transmitted by water contact.
It is an endemic disease in Egypt.

Schistosoma hematobium
• Urinary tract
• Bullinus trancutus snail
• Egypt
Schistosoma mansoni
• Large intestine
• Biomphilaria alexandrina
snail
• Egypt
Schistosoma japonicum
• Large intestine
• Oncomelania snails e.g.
Oncomelaniahupensis
• China

LIFE CYCLE OF SCHISTOSOMIASIS:

 Mode of transmission:
Cercaria in polluted water penetrates skin of new host
during bathing or irrigating lands.
 IP.:
5-8 ws (1-2 ms) from penetration of skin by cercaria till
appearance of eggs in stool or urine.
 Infective stage:
Cercaria “lives 24-72 hs (1-3 ds) in water then dies”.

Clinical picture:
Itching
Dermatitis
“Cercaria
penetration
”
General
weakness
Anemia
Terminal
hematuria
or blood in
faeces
Cystitis
Urethritis
Stone
formation
Colitis
Liver
cirrhosis
Portal HPN
Esophageal
varices &
bleeding
Cancer

DIAGNOSIS
• Suggestive in endemic areas.
• e.g. terminal haematuria or dysentery
C/P
• (a) Microscopic exam.: ova in urine & stools.
• (b) Immunologic tests:
• Complement fixation test: +ve few ws after infection & persists for
many ys.
• Intradermal test: injection of Ag. prepared from adult worms. Reading is
taken within 15 min. +ve reaction signifies infection (past or present).
Lab examination

Spread of schistosomiasis in Egypt
After construction of High Dam
Upper Egypt: S. hematobium is more
prevalent (5-14%) & increased south of
Assuit.
Lower Egypt: S. mansoni is more
prevalent (18-43%) & almost totally
replaced S. hematobium.
Before construction of High Dam
S. hematobium: all over Egypt + low
prevalence south of Assuit.
S. mansoni: Nile delta & Giza Gov.

Change of basin irrigation to perennial irrigation
……...change in velocity & volume of water flow +
decreased silt in water……….affected snail distribution.

ECOLOGY (ENDEMICITY)
Environment
• Unsanitary
environment.
• Lack of safe water
supply for bathing &
washing.
• Unavailable latrines.
• Suitable climate
(temp.+humidity) for
development of cercaria
& snails.
Agent
• Continuous flow of
snail intermediate host
from Nile resources.
• Perennial irrigation
favors development of
snails.
• Cercaria characts. (big
No., survive 2-3 ds,
thermotropic, have great
affinity to man).
Host
• Age: 10-20 ys (swimming
in infected canals in
summer).
• Sex: males (farming &
irrigation).
• Education:↓in educated
persons (avoid polluted
water & seek medical care
early).
• Occupation: farmers &
fishermen.
• Habits & Behavior:
defecation & urination in
canal water.
• Underutilization or
reluctance to seek
medical care.

CONTROL
1ry prevention
• 1. Sanitary water supply &waste
disposal e.g. sanitary latrines.
• 2. Mechanization of agriculture,
irrigation & drainage system.
• 4. Provision of recreation places in
rural areas.
• 5. Snail control:
• Periodic drying of canals.
• Clearance from vegetation.
• Trapping snails.
• Manual collection of snails.
• Molluscicides to kill snails.
Protection of susceptible host
• Health education for:
• 1. Mode of transmission.
• 2. Role of defecation & urination in
canal water.
• 3.Drying of skin after water contact
to kill cercaria before entering skin.
• 4.Wearing PPE on water contact e.g.
gloves & boots.
• 5. Seek medical ttt early when
infected.

Secondary prevention:
Measures for cases
• Early case finding by routine stool &
urine examination for S. eggs at any
occasion of health appraisal, such as:
• (a) Health appraisal of school
children.
• (b) Examination of army recruits.
• (c) Periodic checkup.
• (d) Pre-placement examination.
• (e) All attendants of health services.
• ttt of discovered cases.
• Re-examination to be sure of cure.
• Health education for preventing re-
infection.
• No special measures as there is no
man to man infection; but the
following are recommended:
• Stool & urine examination for early
detection of cases.
• Health education to avoid infection.
• Mass treatment controls reservoir of
infection & limits spread of disease.
Praziquantel (non-antimonial drug)
“orally in a single dose, 30 mg/Kg
BW with a max. of 2400 mg (4
tablets)”.

TREATMENT OF SCHISTOSOMIASIS
Praziquantel (non-antimonial
drug)
• Orally in a single dose, 30 mg/Kg BW
with a max. of 2400 mg (4 tablets).
• Tablets 600 mg as: Distocide tab.,
Biltricide tab., Praziquantel tab.
• Suspension 600 mg/5 ml as: epiquantel
susp.
Commiphora Mukul extract
• Mirazid 300 mg, 2 caps daily on an
empty stomach.

ANCYLOSTOMIASIS
(Hookworm disease)

• Endemic parasitic helminthic disease which is prevalent in
underdeveloped countries.
• More prevalent in Upper than in Lower Egypt.
• Declining due to community development of rural areas &
availability of health services.

Contact of bare skin with
moist contaminated soil
Attached to mucosa by
mouth capsule.
continuously sucking
blood & laying eggs
Ancylostoma duodenale

Period of communicability: untreated cases remain
infective for years.
IP: 6 ws from penetration of skin to appearance of eggs
in stool.
Reservoir of infection: Man: infected person who
discharges eggs in faeces

Clinical picture:
May be asymptomatic.
Ground itch
• Local dermatitis
at site of entry of
larvae.
Respiratory
manifestations
• Migrating larvae
• Patchy lung
consolidation,
Upper respiratory
catarrh.
Anaemia
• Microcytic
hypochromic
“chronic blood
loss by worm
sucking blood”.
General
manifestations
• Retarded physical
growth & mental
development of
children.

DIAGNOSIS:
Suggestive but not
diagnostic.
C/P
Stool exam: 4-cell eggs
Laboratory

ECOLOGY OF ANCYLOSTOMIASIS
Environment
• Unsanitary environment.
• Lack of safe water supply for
bathing & washing.
• Unavailable latrines.
• Suitable climate (temp. &
humidity) for eggs to hatch &
continue life cycle.
Host
• Age: children of
underdeveloped areas.
• Occupation: farmers &
agriculture workers.
• Habits & behavior:
Promiscuous defecation in field
& vicinity of houses.
• Bare foot & getting in contact
with contaminated soil.
• Reluctance of cases to seek
medical ttt & repeated exposure.

CONTROL
I- Prevention:
Community development: safe water supply & sanitary latrines.
Health education: Avoid promiscuous defecation & contamination of soil. Not to
walk bare footed or sit on the soil.
Upgrading of health services.
II. Measures for cases: as bilharzioasis
III. Measures for contacts: non as there is no man to man transmission.

CONTACT SPIROCHETEAL
INFECTIONS

Viral
AIDS
Hepatitis “B&C”
Rabies
Bacterial
Anthrax
Gas gangrene
Gonorrhea
Leprosy
Tetanus
Parasitic
Ancylostomiasis
Schistosomiasis
Spirocheteal
Syphilis

• Spirochaete, treponema pallidum.
• Delicate & is rapidly killed by:
Causative organism
Drying
High
temperature
Disinfectants
Soap &
water

Reservoir: Man: untreated case is infectious during the 1ry & 2ry stages of
disease, usually for 2-4 years.
Exit:
• Exudates of skin & mucous membranes.
• Blood & body fluids (semen, saliva, vaginal & cervical discharge).
IP: About 3 weeks
• Worldwide disease affecting mainly age group from 15-39
• Recently it was found to be increasing.

TRANSMISSION
Contact with open
lesion
• Sexuel contact (Most
important mode).
• Kissing.
• Contact with baby having
congenital syphilis.
• Contact with
contaminated articles.
Congenital infection
• Trans-placental from 4th
month till delivery (not
before as treponema can’t
pass BPB).
Inoculation
infection
• Contaminated blood &
body fluids (contaminated
syringes & needles &
blood transfusion).

Primary syphilis:
• Chancre at portal of entry: firm, indurate, painless & highly
infectious ulcer.
• Enlarged lymph nodes.
• Spontaneously disappears without treatment after 4-6 weeks.

Secondary:
• Generalized skin rash “Patchy lesions of mucous membranes
especially mouth”.
• Involvement of other parts of body.
• Spontaneously disappears within weeks or months followed
after a latent period (years) by the 3rd stage.

Late symptomatic syphilis:
 Reappearance of symptoms.
 Characterized by occurrence of neuro & cardiovascular syphilis
& characteristic lesions involving different parts of body.

History & c/p
Lab investigations
• Dark field microscopic exam
• Serologic testing:
• 1-Non-treponemal test (non-specific): for screening
e.g. Wassermann Reaction (WR) & Venereal Disease
Research Laboratory test (VDRL) “↑false +ve”.
• 2-Treponemal tests (specific test): Use treponema Ag.
e.g. fluorescent treponema antibody absorption test.
DIAGNOSIS

PREVENTION
A. General measures:
B. Specific: Chemoprophylaxis: 1 dose of 2.4 million units of long acting
penicillin I.M. soon after exposure.
Avoidance of sexual promiscuity.
Health education to increase awareness.
Religious & social guidance especially of youth.
Convenient family life & supervision of youth.
Suitable places for leisure time & development of hobbies.
Socioeconomic development & provide facility for marriage.

A. Cases:
1. Early case finding: during survey & on health appraisal:
• Premarital & prenatal examination.
• Exam of food handlers, blood donors, army recruits, child nurses.
• Suspected attendants of medical services.
• Diagnosis of congenital syphilis when mother is syphilitic.
2. Measures for cases:
• Notification confidentially to LHO.
• Isolation: not needed but avoid sexual contact till elimination of infectivity.
• Disinfection: non but precautions with blood & body fluids.

SPECIFIC TREATMENT:
• Long acting penicillin 2.4 million units in a single dose I.M.
• Penicillin sensitive patients: doxycycline 100 mg twice daily for 14 days.
• Re-examination after treatment.

B. Contacts:
• Tracing & Enlistment.
• Examination.
• Surveillance.
• Chemoprophylaxis: 1 dose of 2.4 million units of long acting penicillin I.M.
C. Congenital syphilis:
• Serologic testing & ttt.
• Proper handling of baby with congenital syphilis with caution to avoid
infection.

Contact-transmitted infections

Contact-transmitted infections

Recomendados

Recomendados

Más contenido relacionado

La actualidad más candente

La actualidad más candente (20)

Similar a Contact-transmitted infections

Similar a Contact-transmitted infections (20)

Más de Dalia El-Shafei

Más de Dalia El-Shafei (20)

Último

Último (20)

Contact-transmitted infections