FLOOD

BORNE
DISEASES

CORTEZ
CRUZAT
DAGOHOY
 What is MALARIA?
 Disease caused by protozoan parasites
called Plasmodium.
 It is usually transmitted through the bite
of an infected female Anopheles
mosquito.
 Malaria may also be transmitted
through the following:
 Transfusing blood that is positive for
malaria parasites
 Sharing of IV needles (especially among
IV drug users)
 Trans -placental (transfer of malaria
parasites from an infected mother to her
unborn child)
Female Anopheles mosquito
 Anthropophilic : from humans
 Zoophilic : from animals
 Endophagic : prefer to bite indoors
 Exophagic : prefer outdoor biting

This anopheles mosquito bites from

dusk to dawn and it breeds in clear,
slow flowing streams that are found
in mountainous/forested areas or in
brackish water where salt and fresh
water meet. This is usually found in
coastal areas
What are the common species of
malaria parasites in the Philippines?

 Plasmodium falciparum and Plasmodium vivax are

the common species of malaria parasites in the
Philippines where 70% of malaria cases are P.
falciparum while 29% are P. vivax.
 There are also P. malariae cases but contributes to
about < 1% of the total malaria cases.
P. falciparum
 Causes severe malaria.
 Creates a high level of parasitemia and
sequestration causing end organ damage.
 Sequestration is a specific property.
 Usually seen in the smears are younger forms
before sequestration takes place.
Who are at risk in getting malaria?

 Children
 Pregnant women
 Indigenous peoples
 Forest workers, miners, soldiers
 Persons who are not from a malaria endemic area
but travel to this area
CLINICAL MANIFESTATION
HISTORY TAKING & P.E
 Get a history of recent travel in those patients with
high grade fever.
 Most patients will present with fever and headache.
 Thereis no neck stiffness or photophobia resembling
meningitis.
PHYSICAL EXAMINATION
 Most patients will have splenomegaly.
Diagnosis
Malarial Smear
 In this procedure, a film of blood is placed on a slide, stained, and
examined microscopically.
 Peripheral smear examination for malarial parasite is the gold-standard in
confirming the diagnosis of malaria.
THICK SMEARS THIN SMEARS
More sensitive than thin smears. Less sensitive.
Can’t speciate. Facilitate speciation
Parasitemia can be calculated based on Qualitative test
the number of infected RBC.
Quantitative test.
Can concentrate the parasites increasing
diagnostic sensitivity.
 Quantitative Buffy Coat (QBC) Test
 It involves staining of the
centrifuged and
compressed red cell layer
with acridine orange and its
examination under UV light
source.
 It is fast, easy and claimed
to be more sensitive than
the traditional thick smear
examination.
Rapid Diagnostic Test (RDT)

 This is a blood test for

malaria. It can be
conducted outside the
laboratory and inside the
field.
 It gives a result within 10
to 15 minutes.
 This is done to detect
malarial parasite antigen
in the blood.
TREATMENT
PREVENTION
 Malaria case should be reported.
 A thorough screening of all infected person’s from
mosquitoes is important.
 Mosquito breeding places must be destroyed.
 Homes should be sprayed with effective insecticides
which have residual actions on the wall.
 Mosquito nets should be used especially when in
infected areas.
 Insecticide Treated Bed Nets (ITN’s) have emerged as a
very important tool in malaria control in endemic areas.
What is DENGUE?
 Dengue is due to a flavivirus transmitted by the bite
of the Aedes mosquito. It may be caused by one of
four serotypes.
 There are 4 distinct, but closely related, serotypes
of the virus that cause dengue (DEN-1, DEN-2, DEN-
3 and DEN-4).
 Aedes aegypti
 The Aedes
aegypti mosquito is the
main vector that transmits
the viruses that cause
dengue. The viruses are
passed on to humans
through the bites of an
infective
female Aedes mosquito,
which mainly acquires the
virus while feeding on the
blood of an infected
person.
 TRANSMISSION
 The Aedes aegypti mosquito is the primary
vector of dengue. The virus is transmitted to
humans through the bites of infected female
mosquitoes. After virus incubation for 4–10
days, an infected mosquito is capable of
transmitting the virus for the rest of its life.

 Infected symptomatic or asymptomatic

humans are the main carriers and multipliers
of the virus, serving as a source of the virus
for uninfected mosquitoes. Patients who are
already infected with the dengue virus can
transmit the infection (for 4–5 days;
maximum 12) via Aedes mosquitoes after
their first symptoms appear.
 The Aedes aegypti mosquito lives in urban
habitats and breeds mostly in man-made
containers. Unlike other mosquitoes Ae.
aegypti is a day-time feeder; its peak
biting periods are early in the morning
and in the evening before dusk.
Female Ae. aegypti bites multiple people
during each feeding period.
Primary infection
 Primary infection is characterized by fever, break
bone fever, retro-orbital pain and flue like
syndrome.
 The person who is not previously infected with any
Flavivirus is termed as primary infection.
 In primary infection ratio of Dengue specific IgM to
IgG is high.
Secondary infection

 Dengue infection in host who is immunologically

sensitized to dengue or other flavivirus is termed as
secondary infection.
 Secondary infection is characterized by rise in
antibody titer. The ratio of IgM to IgG is low.
CLINICAL MANIFESTATION
Classical dengue fever
 It is characterized by fever,
rashes, severe headache, pain
behind eyes, pain in muscle
and joints, enlarged lymph
nodes,
 Fever lasts for 2-7 days
 Myalgia and break bone
fever ( deep bone pain) is the
characteristic of Dengue fever
 Classical dengue fever is self-
limited.
 Mostly adults and older
children are affected,
Dengue hemorrhagic fever (DHF
 DHF is marked by bleeding from skin and mucus
membrane.
 DHF has four major clinical manifestation- High fever,
hemorrhagic phenomenon, hepatomegaly and
circulatory failure.
 In early stage of infection DHF resembles classical
dengue fever.
 Usually occurs in children
 About 23% of children with DHF develops circulatory
failure with haemo-concentration and a marked
decrease in platelets counts leading to severe
hemorrhage.
Dengue shock syndrome (DSS)
 DSS is serious form of DHF.
 All serotypes of Dengue are associated with DHF and DSS.
 The cause of DSS is not clearly understood. But it is assumed
due to antibody dependent enhancement (ADE).
 From recent outbreak information of DHF, patients infected
with DEN-2 after primarily infected with other serotypes can
leads to DSS.
 DSS is characterized by circulatory failure, rapid pulse,
abnormal pain, severe bleeding from GI tract and other
organs.
 Usually occurs in children
DIAGNOSTIC TEST
 VIRUS ISOLATION
 Before day 5 of illness, during the febrile period,
dengue infections may be diagnosed by virus
isolation in cell culture, by detection of viral RNA by
nucleic acid amplification tests (NAAT), or by
detection of viral antigens by ELISA or rapid tests.
Virus isolation in cell culture is usually performed
only in laboratories with the necessary infrastructure
and technical expertise.
IgM-capture enzyme-linked
immunosorbent assay (MAC-ELISA)
 MAC-ELISA has been widely used in the past few years.
It is a simple test that requires very little sophisticated
equipment. MAC-ELISA is based on detecting the
dengue-specific IgM antibodies in the test serum by
capturing them using anti-human IgM that was
previously bound to the solid phase.
 This is followed by addition of dengue antigen if the
IgM antibody from the patient's serum is anti-dengue, it
will bind to the dengue antigen. An enzyme substrate is
added to give a colour reaction for easy detection
 Nucleic acid detection assays with excellent
performance characteristics may identify dengue viral
RNA within 24–48 hours. However, these tests require
expensive equipment and reagents and, in order to
avoid contamination, tests must observe quality control
procedures and must be performed by experienced
technicians.
 NS1 antigen detection kits now becoming commercially
available can be used in laboratories with limited
equipment and yield results within a few hours. Rapid
dengue antigen detection tests can be used in field
settings and provide results in less than an hour.
TREATMENT AND MANAGEMENT
A Probable dengue
DENGUE CASE MANAGEMENT
S Live in/travel to dengue endemic area.
S Fever and 2 of the following criteria
E • Nausea, vomiting
S • Rash Warning signs
S • Aches and pains • Abdominal pain or tenderness
M • Tourniquet test positive • Persistent vomiting
E • Leukopenia • Clinical fluid accumulation
N • Any warning sign • Mucosal bleed
T Laboratory-confirmed dengue • Lethargy, restlessness
(Important when no sign of plasma leakage) • liver enlargement >2cm
C • Increase in HCT concurrent w/ rapid
L decrease in platelet count
A
S
S
I
F NEGATIVE POSITIVE
I Co-existing conditions
C Social circumstances Dengue w/ warning
A signs
Severe dengue
T
(-) (+)
I
O Group B Group C
N Group A
GROUP B
GROUP C
5/7/2019
 To discuss the etiologic agent, mode of transmission
and clinical manifestations of typhoid and cholera
 To know the different stages of typhoid fever
 To discuss the epidemiology of typhoid and
cholera
 To discuss the prevention, treatment and
management
  Typhoid fever is a life-threatening infection caused by the bacterium
Salmonella Typhi.
 It is usually spread through contaminated food or water.
 Symptoms include prolonged fever, fatigue, headache, nausea,
abdominal pain, and constipation or diarrhoea. Some patients may
have a rash. Severe cases may lead to serious complications or even
death.
 Typhoid fever can be treated with antibiotics although increasing
resistance to different types of antibiotics is making treatment more
complicated.
 Two vaccines have been used for many years to prevent typhoid. A
new typhoid conjugate vaccine with longer lasting immunity was
prequalified by WHO in December 2017.

5/7/2019
 Gram negative
 Non- spore former
 Facultatively anaerobe
bacilli
 2-3um by 0.4- 0.6 um
 2 types of salmonellosis
 Enteric typhoid fever
 Salmonella typhi
 Salmonella paratyphi

 The growth of these serotypes is restricted to human hosts,

in whom these organisms can cause enteric typhoid (fever)
 Non- typhoidal – can colonize the gastrointestinal tract 0f a
broad range animals, including mammals, reptiles, birds,
and insects.
 The disease is communicable for as long as the infected person
excretes S.typhi in their excreta, usually after the 1st week of
illness through convalescence.

 Approximately 10% of untreated cases will excrete S. typhi for

3 months and between 2-5% of all cases become chronic
carriers.
 consumption of contaminated food or water
 direct faecal–oral transmission may occur
 shellfish taken from sewage-polluted areas are an
important source of infection
 through eating raw fruit and vegetables fertilized by
human excreta and through ingestion of contaminated
milk and milk products
 flies
 pollution of water
5/7/2019
 WHO estimates the global typhoid fever disease burden at
11-20 million cases annually, resulting in about 128 000–161
000 deaths per year.
 Typhoid risk is higher in populations that lack access to safe
water and adequate sanitation. Poor communities and
vulnerable groups including children are at highest risk.
 Recent data from south
Asia indicate that the
presentation of typhoid
may be more dramatic in
children younger than 5
years, with higher rates of
complications and
hospitalization
Southeast Asia:
Annual incidence: 24/100 000 person years in Vietnam, 180/100
000 person years in Indonesia, 494/100 000 person years in India.

 420 000 deaths occur annually

 Without treatment, case-fatality rates of infection are 10%.
 With appropriate antibiotic therapy, case-fatality rates can be
reduced to below 1%.
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 Culture
 Rapid diagnostic tests
 PCR
 Other nonspecific laboratory tests:
 Complete blood count
 Urinalysis
 Liver function test
5/7/2019
 The ideal time of doing a
blood culture is when the
patient is having chills (and
not when the fever spikes,
as is commonly thought).
 Blood for culture should be
taken before giving the first
dose of antibiotics.
the limitations of laboratory media;
the presence of antibiotics;

the volume of the specimen cultured; or

the time of collection

 Less sensitive for diagnosis of infection among children as

compared to adults

 Positive in only 40-60% of cases, usually early in the

course of the disease

 Expensive and requires specialist facilities and personnel

 55–90% sensitive

 Limitations in use
 Although the most sensitive, it is an invasive procedure, and cannot be
performed outside specialist settings
 Has limited clinical value, especially in ambulatory management
 The specimen is difficult to obtain
 Stool culture can help in detecting typhoid carriers.
Stool should be collected from acute patients in a
sterile wide-mouthed plastic container and should
preferably be processed within two hours of
collection.
 The choice of agar media includes Mac Conkey agar,
desoxycholate citrate agar, xylose-
lysinedesoxycholate agar, and hektoen enteric agar
or SS (SalmonellaShigella).
 an agglutination test which
detects the presence of serum
agglutinins (H and O) in patients
serum with typhoid and
paratyphoid fever.
 When facilities for culturing are
not available, the Widal test is
the reliable and can be of value
in the diagnosis of typhoid fevers
in endemic areas.
 The Widal test can be
conducted in two ways

A. Slide agglutination Widal test

1. Qualitative Slide Test
2. Quantitative Slide Test
B. Tube agglutination Widal test
 Previous typhoid vaccination may contribute to elevated
agglutinins in the non-infected population.
 Cross reaction between malaria parasites and salmonella
antigens may cause false positive Widal agglutination test
 False positive Widal tests have also been reported for
patients with non-enteric salmonella infection, for example
Typhus, Immunological disorders, chronic liver disease and
cryptococcal meningitis
 Prior use of antibiotics as seen with the widespread
antibiotic abuse can dampen antibody response giving a low
titre in the Widal test even in the face of bacteriologicially
confirmed typhoid fever resulting in misdiagnosis
 an antibody-detection test that is user-friendly
and can be used at the point of care.
 This simple one-step rapid test can be
performed in just two minutes.
 The test is as simple and fast as the slide latex
agglutination tests but has been modified to
improve the sensitivity and specificity to 75-85%
and 75-90%, respectively.
 The O9 antigen used in the test is extremely
specific, and can detect IgM O9 antibodies
within minutes.
 A positive result is a definite indicator of a
Salmonella infection
 rapid-dot enzyme immunoassay (EIA) that takes about
three hours to perform.
 detects IgG and IgM antibodies to a specific 50 kD outer
membrane protein (OMP) antigen of S. typhi.
 Detection of IgM signifies acute enteric in the early phase
of infection while detection of both IgG and IgM indicates
acute enteric in the middle phase of infection.
 The test becomes positive right in the first week of fever
and the results are available within one hour.
 Thus, it is faster than blood culture and Widal, in which
results take 48 and 18 hours, respectively.
 IgM dipstick test is based on the detection of S. typhi-specific IgM
antibodies in serum or whole blood samples.
 Specific antibodies appear a week after onset of symptoms and
signs — this fact should be kept in mind while interpreting a
negative serological test.
 Polymerase chain reaction (PCR) has been used for the
diagnosis of typhoid fever with varying success.
 Nested PCR, which involves two rounds of PCR using two
primers with different sequences within the H1-d flagellin
gene of S typhi, offers the best sensitivity and specificity.
 Combining assays of blood and urine, this technique has
achieved a sensitivity of 82.7% and reported specificity of
100%.
 However, no type of PCR is widely available for the clinical
diagnosis of typhoid fever.
Complete  Leukopenia and neutropenia - 15-
blood 25% of cases
count  Leukocytosis - common in children,
common during the first 10 day of
illness, in cases complicated by
intestinal perforation or secondary
infection
 Thrombocytopenia
 Normochromic anemia
 Hypochromia if with blood loss
Urinalysis transient albuminuria

Liver function test moderate elevation of

enzymes
 Public Private

 300.00  1385.00++
95
INTESTINAL BLEEDING
•Administration of antibiotics for 10 to 14 days.

•Significant blood loss may need to be replaced by blood transfusion.

•The patient is kept in hospital for 5 to 7 days after the bleeding has completely
stopped.

Source: World Health Organization

Ifperforation is confirmed, surgical repair should not be
delayed longer than six hours.

Metronidazole and gentamicin or ceftriaxone should be

administered before and after surgery if a fluoroquinolone is
not being used to treat leakage of intestinal bacteria into the
abdominal cavity.

Source: World Health Organization

If typhoid meningitis is suspected, the patient should
immediately be treated with Dexamethasone (an
initial dose of 3 mg/kg by slow IV infusion over 30
minutes followed by 8 doses of 1 mg/kg every 6 hours)
with Chloramphenicol.

Source: World Health Organization

In order to eradicate S. typhi carriage
Amoxicillin or ampicillin (100 mg per kg per day) plus probenecid
(Benemid®) (1 g orally or 23 mg per kg for children) or TMP-SMZ (160 to
800 mg twice daily) is administered for six weeks.

Clearance of up to 80% of chronic carriers can be achieved with the

administration of 750 mg of Ciprofloxacin twice daily for 28 days.

Source: World Health Organization

Chronic carriers should be excluded from any
activities involving food preparation and serving.

Food handlers should not resume their duties until

they have had three negative stool cultures at least
one month apart.

Source: World Health Organization

WHO, CDC

5/7/2019
Source: Center For Disease Control And Prevention
Travelers to areas where there is moderate to high risk of exposure to S.
typhi

Laboratory workers who deal with S. typhi

Household contacts of known S. typhi carriers

Source: World Health Organization

Center For Disease Control And Prevention
1. Safe Disposal of Feces
 Appropriate facilities for human waste disposal must be
availablefor all the community.

 Collection and treatment of sewage, especially during

the rainy season, must be implemented.

 In areas where typhoid fever is known to be present,

the use of human excreta as fertilisers must be
discouraged.
Source: World Health Organization
2. Hand washing
Hands readily become
contaminated with fecal material after
going to the toilet or cleaning children’s
bottoms.

Rinsing fingers with water alone is not

enough. Hands need to be well washed
after contact with feces; rubbed with
soap.

Source: World Health Organization

3. Keeping water clean
The main preventive measure is to ensure access to safe water.

The water needs to be of good quality and must be sufficient to supply

all the community with enough drinking water as well as for all other
domestic purposes such as cooking and washing.

During outbreaks the following control measures are of particular

interest:
In urban areas, control and treatment of the water supply systems must
be strengthened
Inrural areas, wells must be checked for pathogens and treated if
necessary.

At home, a particular attention must be paid to the disinfection and

the storage of the water.
- Drinking
water can be made safe by boiling it for one minute.

In some situations, such as poor rural areas in developing countries

or refugee camps, fuel for boiling water and storage containers may
have to be supplied.

Source: World Health Organization

4. Fly control
Though flies can carry
microbes from feces to food, fly
control is difficult to achieve.
 If stools are disposed of in toilets or
latrines and these latrines have
covers, then fly-based disease
transmission will be minimized.
5. Food hygiene
“Boil it, cook it, peel it, or forget it”

Ifyou drink water, buy it bottled or bring it to a rolling boil for 1 minute before
you drink it.

Ask for drinks without ice unless the ice is made from bottled or boiled water.

Avoid popsicles and flavored ices that may have been made with contaminated
water.

Eat foods that have been thoroughly cooked and that are still hot and steaming.
Avoid raw vegetables and fruits that cannot be peeled. Vegetables like
lettuce are easily contaminated and are very hard to wash well.

When you eat raw fruit or vegetables that can be peeled, peel them
yourself. Do not eat the peelings.

Avoid foods and beverages from street vendors. It is difficult for food to
be kept clean on the street.

Source: Center For Disease Control And Prevention

World Health Organization
• The program covers diseases of a parasitic, fungal,
viral, and bacteria in nature, usually acquired
through the ingestion of contaminated drinking
water or food.

• The approaches to control and prevention is

centered on public health awareness regarding
food safety as well as strengthening treatment
guidelines.
 Cholera is an intestinal
infection caused by Vibrio
cholerae
 The hallmark of the
disease is profuse
secretory diarrhea
 Although the disease may
be asymptomatic or mild,
severe cholera can cause
dehydration and death
within hours of onset
 Cholera is transmitted by the
fecal-oral route
 Definitive diagnosis is not a
prerequisite for the treatment
of patients with cholera
 The priority in management of
any watery diarrhea is
replacing the lost fluid and
electrolytes and providing an
antimicrobial agent when
indicated

117
 The 19th century English physician John Snow provided the first
demonstration that the transmission of cholera was significantly reduced
when uncontaminated water was provided to the population
 Although not the first description, the discovery of the cholera organism
is credited to German bacteriologist Robert Koch, who independently
identified V cholerae in 1883 during an outbreak in Egypt
 Since 1817, 7 cholera pandemics have occurred

118
 The seventh pandemic of cholera, and the first in the 20th century,
began in 1961; by 1991, it had affected 5 continents
 A new strain of cholera, V cholerae serogroup O139 (Bengal)
emerged in the fall of 1992 and caused outbreaks in Bangladesh
and India in 1993
 Epidemics occur after war, civil unrest, or natural disasters when
water and food supplies become contaminated with V cholerae in
areas with crowded living conditions and poor sanitation

119
 comma-shaped
 gram-negative aerobic or
facultatively anaerobic
bacillus
 1-3 µm in length by 0.5-
0.8 µm in diameter
 antigenic structure
consists of a flagellar H
antigen and a somatic O
antigen
120
 To reach the small
intestine, however, the
organism has to negotiate
the normal defense
mechanisms of the GI
tract
 The infectious dose of V
cholerae required to
cause clinical disease
varies by the mode of
administration
121
 V cholerae O1 and V cholerae O139 cause clinical disease by
producing an enterotoxin that promotes the secretion of fluid and
electrolytes into the lumen of the small intestine
 The enterotoxin is a protein molecule composed of 5 B subunits and
2 A subunits
 Fluid loss originates in the duodenum and upper jejunum; the ileum
is less affected

122
 Cholera can be an endemic, epidemic, or a pandemic disease.
Initiation and maintenance of epidemic and pandemic disease by V
cholerae result from human infection and poor sanitation with
assistance from human migration and seasonal warming of coastal
waters
 V cholerae is a saltwater organism, and its primary habitat is the
marine ecosystem where it lives in association with plankton
 Cholera has 2 main reservoirs, humans and water
 Primary infection in humans is incidentally acquired
 Secondary transmission occurs through fecal-oral spread of the
organism through person-to-person contact or through
contaminated water and food
123
 During 2016, 132 121 cases were notified from 38 countries,
including 2420 deaths
 An estimated 2.9 million cases and 95,000 deaths occur each year
around the world
 Approximately one in 10 (10%) infected persons will have severe
disease characterized by profuse watery diarrhea, vomiting, and leg
cramps
 Data from ProMed and surveillance revealed 42,071 suspected and
confirmed cholera cases reported from 2008 to 2013, among which
only 5,006 were confirmed
 The average annual incidence in 2010–2013 was 9.1 per 100,000
population 124
2019/5/7
 Profuse watery diarrhea is a hallmark of cholera
 Vomiting, although a prominent manifestation, may not always be
present
 The diarrhea and vomiting lead to isotonic dehydration
 Hypoglycemia is the most common lethal complication of cholera in
children
 Acidemia
 Hypokalemia results from potassium loss in the stool, with a mean
potassium concentration of approximately 3.0 mmol/L
3-5% loss of normal body weight - Excessive thirst
5-8% loss of normal body weight - Postural hypotension, tachycardia,
weakness, fatigue, dry mucous membranes or dry mouth
>10% loss of normal body weight - Oliguria; glassy or sunken eyes;
sunken fontanelles in infants; weak, thready, or absent pulse; wrinkled
"washerwoman" skin; somnolence; coma

130
 Stool Exam
 Routine differential media
 Alkaline enrichment media
 Serotyping and Biotyping
 Hematologic Test
1. Assess for dehydration
2. Rehydrate the patient and monitor frequently, then reassess
hydration status
3. Maintain hydration; replace ongoing fluid losses until diarrhea
stops
4. Administer an oral antibiotic to the patient with severe
dehydration
5. Feed the patient

133
  Water and sanitation
interventions
 Hygiene promotion and
social mobilization
 Oral cholera vaccines

5/7/2019
  In 2014 the Global Task Force on Cholera Control (GTFCC), with its
Secretariat based at WHO, was revitalised. The GTFCC is a network of
more than 50 partners active in cholera control globally, including
academic institutions, non-governmental organisations and United
Nations agencies.
 Through the GTFCC and with support from donors, WHO works to:
 promote the design and implementation of global strategies to
contribute to capacity development for cholera prevention and
control globally;
 provide a forum for technical exchange, coordination, and cooperation
on cholera-related activities to strengthen country capacity to prevent
and control cholera;

5/7/2019
  support countries for the implementation of effective cholera
control strategies and monitoring of progress;
 disseminate technical guidelines and operational manuals;
 support the development of a research agenda with
emphasis on evaluating innovative approaches to cholera
prevention and control in affected countries; and
 increase the visibility of cholera as an important global public
health problem through the dissemination of information
about cholera prevention and control, and conducting
advocacy and resource mobilization activities to support
cholera prevention and control at national, regional, and
global levels.
5/7/2019
  In October 2017, GTFCC partners launched a strategy for
cholera control Ending Cholera: A roadmap to 2030. The
country led strategy aims to reduce cholera deaths by 90%
and to eliminate cholera in as many as 20 countries by 2030.

5/7/2019
  Early detection and quick response to contain outbreaks: the
strategy focuses on containing outbreaks—wherever they
may occur— through early detection and rapid multisectoral
response including community engagement, strengthening
surveillance and laboratory capacity, health systems and
supply readiness, and establishing rapid response teams.
 A targeted multi-sectoral approach to prevent cholera
recurrence: the strategy calls on countries and partners to
focus on cholera “hotspots”, the relatively small areas most
heavily affected by cholera. Cholera transmission can be
stopped in these areas through measures including improved
WASH and through use of OCV.

5/7/2019
  An effective mechanism of coordination for technical
support, advocacy, resource mobilisation, and partnership at
local and global levels: The GTFCC provides a strong
framework to support countries to intensify efforts to control
cholera, building upon country-led cross-sectoral cholera
control programs and supporting them with human,
technical, and financial resources.

5/7/2019
 Leptospirosis
• Leptospirosis is a zoonotic disease with epidemic
potential, especially after heavy rainfall. It occurs
throughout the world and is emerging as an important
public health problem in both tropical and subtropical
countries, affecting mostly vulnerable populations.
Humans usually acquire leptospirosis through direct
contact with the urine of infected animals or a urine-
contaminated environment.
• Leptospirosis is a disease that is caused by spirochete
bacteria in the genus Leptospira. There are 10
pathogenic species, and more than 250 pathogenic
serovars.
 Pathogen
• Order: Spirochaetales
• Family: Leptospiracea
• Genus: Leptospira
• Species:
– pathogenic ex. L. interrogans
– saprophytic ex. L. biflexia
• 7 more common pathogenic species identified
w/ 250 serovar
 Leptospire
Pathogenic Saprophytic
• Maintained in nature in the • Found in many types of wet
renal tubules of certain or humid environments
animals ranging from surface waters
• Natural maintenance hosts and moist soil to tap water
• Can be distinguish form each • Saprophytic halophilic (salt-
other through antigenic loving) leptospires are found
makeup (serogroup & in seawater
serovar)
 Pathogen
• Gram (-) spiral bacterial (corkscrew) w/ end
hooks & paired axial flagella
• Finely coiled, thin, motile, continuously
spinning on its axis
• Too thin to be seen in ordinary microscopy
• Obligate slow growing anaerobes
• Survive best for months in freshwater, damp
alkaline soil, vegetation & mud w/
temperature >22ºC
 Epidemiology
• While leptospirosis occurs worldwide, it is more
common in tropical or sub-tropical climates.
• It is estimated that more than 1 million cases occur
worldwide annually, including almost 60,000 deaths.
• In the United States, approximately 100–150
leptospirosis cases are reported annually. Puerto Rico
reports the majority of leptospirosis cases, followed by
Hawaii.
• Outbreaks of leptospirosis tend to occur after heavy
rainfall or flooding in endemic areas, especially areas
with poor housing and sanitation conditions.
 Epidemiology
• In the Philippines, a total of 2,495
leptospirosis cases were reported nationwide
from January 1 to December 2, 2017, which is
49.1% higher compared to the same period
last year (1,673).
• Most of the cases were from the following
regions: NCR (19.2%), Region VI (19%), Region
I (14.8%), Region III (8.3%), and Region II
(6.5%).
 Reservoir - Mammals
• Wild animals
– The primary reservoir of most leptospira variants
which in turn infect domestic animals
– Can persist in animal renal tubules for
months/years without causing pathologic changes
– Urinary shedding/leptospiruria is the most
important origin of contamination
– Rats most common source worldwide
 Natural maintenance Host & the
common serovar involve:
• RAT
– Serovar icterohaemorrhagica & copenhageni, L.
balum
• Cattle
– Serovar hardjo
• Dogs
– Serovar canicola
• Other domestic animal
 Transmission
• Leptospires are spread by the urine of infected animals (rodents,
dogs, livestock, pigs, horses, wildlife).
• The bacteria can survive for weeks to months in urine-
contaminated water and soil.
• People can be infected through
– Direct contact with the urine or reproductive fluids from infected
animals » Contact with urine-contaminated water (floodwater, rivers,
streams, sewage) and wet soil
– Ingestion of food or water contaminated by urine or urine-
contaminated water
• Transmission occurs through mucous membranes, conjunctiva, and
skin cuts or abrasions.
• Human-to-human transmission is very rare but has been
documented through sexual intercourse and breastfeeding.
Transmission has also rarely occurred through animal bites.
 Transmission
• High-risk activities can include wading,
swimming, or boating in floodwater or freshwater
(rivers, streams, lakes) that may be contaminated
with animal urine. Some actions like prolonged
immersion in, submerging head in, or swallowing
contaminated water can particularly increase risk.
• Other high risk activities can include direct
contact with animals and activities that can lead
to skin abrasions and water or soil exposure, such
as clearing brush, trekking, and gardening.
 Pathophysiology
• Entry  leptospermia  multiple in the small
blood vessel entdothelium in any part of the
body but particularly affects the liver & kidney
• In the kidney  interstitium  renal tubules
– Interstitial nephritis
– Tubular necrosis leading to renal failure or it may
not cause significant damage
 Pathophysiology
• In the liver
– Centrilobar necrosis w/ proliferations of Kupffers cells
and hepatocellular  dysfunction and jaundice
• Skeletal muscles
– Microcirculation is impaired & capillary permeability
increased  leakage & circulatory hypovolemia
– Edema, vascuolization of myofibrils, necrosis
• Disseminated vasculitis syndrome - severe cases
• Eyes – invade the aqueous humor where they can
persist for months causing uveitis
 Clinical Findings
• Incubation period is 2–30 days; most illnesses occur
5–14 days after exposure.
• Symptoms can include fever, headache, myalgia
(typically of the calves and lower back), conjunctival
suffusion, nausea, vomiting, diarrhea, abdominal
pain, cough, and sometimes a skin rash.
• Severe symptoms can include jaundice, renal failure,
hemorrhage (especially pulmonary), aseptic
meningitis, cardiac arrhythmias, pulmonary
insufficiency, and hemodynamic collapse. Combined
renal and liver failure associated with leptospirosis is
referred to as Weil’s disease.
 Clinical Findings
• 2 clinical syndrome
– Mild anicteric form (90%)
• Usually biphasic
• Self limiting and mortality is rare
– Severe icteric form
• Phase maybe continuous, indistinguishable &
characterized by multiorgan involvement & even failure
• 5-10% mortality
 Mild Anicteric Phase
• 2 clinical stages/phase
– 1st phase/septicemic/leptospiremic
– 2nd phase/immune/leptospiruric
• Often the transition between the stages is
obscured
• Patient’s condition can deteriorate suddenly at
any time
1st phase/septicemic/leptospiremic
• Last for 407 days
• Flu-like syndrome- abrupt onset of fever, chills,
weakness, myalgia primarily the calves, back &
abdomen
• Other s/s: sore throat cough, chest pain,
hemoptysis, rash, frontal headache, photophobia,
mental confusion & other symptoms of
meningitis
• Leptospira can be isolated from blood, CSF &
most tissues
1st phase/septicemic/leptospiremic
• Physical findings:
– Fever
– Subconjunctival suffusion
– Pharyngeal congestion
– Mild jaundice
– Lymphadenopathy
– Muscle tenderness (calf muscles & low back) abdominal
muscle mimic acute abdomen
– Splenomegaly
– Hepatomegaly
– Rash (macular, maculopapular, erythematous, urticarial,
hemorrhagic)
 2nd phase/immune/leptospiruric
• Follows after 1-3 days of improvement from
septicemic phase
• Occurs as a consequence of the
immunological response to leptospira infxn &
last for 0-30 days
• Nonspecific symptoms are less severe lasting
for few days or weeks
• Antibody to leptospira can be detected
• Leptospira can be isolate from the urine
 2nd phase/immune/leptospiruric
• S/s are more specific & referable to infected organs such as the
meninges, liver, kidneys & eyes
• Aseptic meningitis- most important clinical syndrome in the
immune anicteric stage
– Herald by: severe headaches (77%), meningeal symptoms (50%)
– Cranial nerve palsies, encephalitis & changes in the level of
consciousness (less common)
– Last for few days (1-2 wks)
• Renal: azotemia, pyuria, hematuria, proteinuria, oliguria (50%)
• Liver: jaundice, hepatomegaly, abdominal pain/tenderness, signs of
coagulopathy
• Pulmonary: (20-70%) cough, dyspnea, chest pain, hemoptysis
– Benign however it can be fetal as a result of pulmonaty hemorrhage or
ARDS
– Occurs in icteric and anicteric form
 2nd phase/immune/leptospiruric
• Ocular: subconjunctival hemorrhages, uveitis,
chorioretinitis
• Hematologic: bleeding, petechiae, purpura,
ecchymosis, splenomegaly, abdominal tenderness
• Cardiac: myocarditis with signs of congested heart
failure, pericarditis
• Pancreas: pancreatitis
• Gastrointestinal: hematocheziaor just occult blood
positive stool, abdominal pain, diarrhea/constipation,
n/v
• Muscle: rhabdomyolysis, increase CPK
 Weil disease/severe leptospirosis
• Criteria to determine the dev’t of Weil dse are
not well defined
• Occurs at the end of the 1st stage and peaks in
the 2nd stage
– Fever may be marked
– Patients w/ severe jaundice are more likely to develop
renal failure, hemorrhage & cardiovascular collapse
• Vascular & renal dysfunction accompanied by
jaundice develop 4-9 days after the onset of dse
& jaundice may persist for wks
 Weil disease/severe leptospirosis
• Late sequelae
– Chronic fatigue
– Neuropsychiatric symptoms, uveitis & iridocyclitis
• Outcome during prenangy
– Fetal death
– Abortion
– Stillbirth
– Congenital leptospirosis
 Prognosis
• Weil syndrome: mortality rate of 5-10%
– The most severe cases w/ hepatorenal involvement and
jaundice, have a case-fatality rate of 20-40%
– Pulmonary & renal dysfunction is the most determinant of
prognosis
– Advanced age, clinically evident pulmonary involvement,
elevated serum creatinine level, oliguria & thrombocytopenia
assoc w/ poor prognosis
• Cause of Death
– Renal failure
– Cardiopulmonary failure
– Widespread of haemorrhage
– Liver failure is rare, despite the present of jaundice
 Treatment
• Early treatment may decrease the severity and duration of
disease. In patients with a high clinical suspicion of
leptospirosis, initiating antibiotic treatment as soon as
possible without waiting for laboratory results is
recommended.
• For patients with mild symptoms, doxycycline is the drug of
choice (100 mg orally, twice daily), if not contraindicated.
Other options include azithromycin (500 mg orally, once
daily), ampicillin (500-750 mg orally, every 6 hours),
amoxicillin (500 mg orally, every 6 hours).
• For patients with severe disease, IV penicillin is the drug of
choice (1.5 MU IV, every 6 hours), and ceftriaxone (1 g IV,
every 24 hours) can be equally effective.
 Diagnostics
• Antibodies for leptospirosis develop between 3-10 days after symptom
onset, thus any serologic test must be interpreted accordingly – negative
serologic test results from samples collected in the first week of illness do
not rule out disease, and serologic testing should be repeated on a
convalescent sample collected 7-14 days after the first.
• In the acute phase of illness, leptospires are present in the blood
(septicemia) for approximately the first 4–6 days of illness. Leptospires
may be shed intermittently in the urine after approximately the first week
of illness onset. Due to the transience of leptospires in body fluids, a
negative PCR test does not rule out leptospisosis.
• It is best to submit as many specimen types as possible. Recommended
specimens based on collection timing:
– Acute illness (first week): whole blood and serum
– Convalescent illness (after first week): serum +/- urine
Diagnostics
 Prevention
• The first line of leptospirosis prevention is to avoid exposure.
• Avoid wading, swimming, bathing, swallowing, or submersing head in potentially
contaminated freshwater (rivers, streams) especially after periods of heavy rainfall
or flooding.
• Avoid contact with floodwater, and do not eat food contaminated with floodwater.
• If exposure cannot be avoided, wear appropriate personal protective equipment
(PPE) (rubber boots, waterproof coveralls/ clothing, gloves). Cover open wounds
with waterproof dressings.
• Treat unsafe or potentially contaminated drinking water by boiling or chemically
treating.
• Keep rodent populations (rats and mice) or other animal pests under control. Do
not eat food that may have been exposed to rodents and possibly contaminated
with their urine.
• Some studies have shown that chemoprophylaxis with doxycycline might be
effective in preventing clinical disease and could be considered for people at high
risk and with short-term exposures.
 Hepatitis A
• Formerly Enterovirus 72 in the Picornavirus family
• A picornavirus, the prototype of genus
Hepatovirus
• New genus: Heparnavirus
• Spread by fecal-oral route
• Incubation period:15-50 days
• Period of communicability: before to after
symptoms appear
 Epidemiology
• In the Philippines, a total of 422 Hepatitis A cases reported
nationwide from January 1 to December 2, 2017. Among
which , 1 death was reported (CFR=0.24%) This is 34.67%
lower compared to the same time period last year (646).
• Most of the cases were from the following regions: Region
VII (25.83%), Region VI (13.98%), Region X (12.56%), NCR
(10.43%), and Region IV-A (6.16%).
• Ages of cases ranged from less than 1 month to 90 years
old (median=25 years). Majority of the confirmed cases
were male (63%). The most affected age group were from
16 to 20 years (18%).
• A total of 422 (100%) samples were reactive for IGM anti-
HAV.
 Structure
• Naked, icosahedral capsid
• (+) VPg protein (VP1 to VP4)
• Single-stranded RNA, linear, positive-sense
• Only one serotype
 Replication
• Replicates in the cytoplasm
• Interacts with HAVCR-1 expressed on liver and
T cells
• HAV is not cytolytic and released by exocytosis
• Reservoirs: Humans, rarely chimpanzees and
other primates
• Mode of Transmission: Direct and indirect
person-to-person spread via the fecal-oral
route. Rarely, blood-borne transmission can
occur during the viremic phase of the disease.
• Incubation Period: Range 15-50 days; average
28-30 days
• Period of Communicability: Most infectious from
1-2 weeks before symptom onset to about two
weeks after non-jaundice symptom onset or one
week after onset of jaundice. HAV replicates in
the liver and is shed in high concentrations in
feces from 2 weeks before to 1 week after the
onset of clinical illness. The greatest amount of
viral shedding occurs 2 weeks prior to symptom
onset. Infants and children, however, may shed
virus for up to 6 months after infection.
• Susceptibility: Groups at increased risk for
hepatitis A or its complications include
international travelers, MSM, and users of
illegal drugs. Outbreaks of hepatitis A have
also been reported among persons working
with hepatitis A–infected primates. Other risk
factors include sexual or household contact
with an infected person, and contact with a
child or employee in child care. Immunity
after infection lasts for life.
• Resistance:
– Resistant to inactivation by heat at 60˚ for 1 hour
– Ether and acid at pH3
– Not affected by anionic detergent
– Survives prolonged storage at 4˚
– Not inactivated by freezing
– Inactivated by:
• boiling for 1 min
• 1:4000 formaldehyde at 37˚ for 72 hours
• Chloride 1ppm for 30 mins
 Clinical features
• Abrupt onset, with fever, malaise, anorexia,
nausea, abdominal discomfort, vomiting and,
sometimes, diarrhea. Jaundice, dark urine and
clay-colored stool follow a few days later.
Infections range from asymptomatic to disabling
illness that may last several months but is seldom
fatal and not chronic. Typically, symptom severity
increases with age and duration of infection is
several weeks. Prolonged, relapsing symptoms
may occur for up to 6 months to 1 year in about
15% of cases.
• PRODOMAL OR PREICTERIC PHASE
– Abdominal pain, malaise, fatigue, joint pain, high
grade fever, loss of appetite, hepatomegaly
• ICTERIC PHASE
– Jaundice (skin, sclera, mucus membranes)
– Cause: elevated bilirubin
– Dark urine
– Pale stool
 Pathogenesis
• Entry from mouth
• The virus replicates in the gastrointestinal tract and spreads
to the liver via blood, viral replication in the liver
• Hepatocytes are infected but no cytopathic effect on
hepatocytes has been observed
• Cytotoxic T cells produced during the immunological
reaction cause the damage which is repaired, infection
clears and no chronicity develops
• In acute phase of the disease IgM antibodies appear-
diagnostic, followed by the appearance of IgG antibodies –
make the person immune to further infection
• If travel to a HAV endemic area within 3
months of symptom onset, classify as
imported.
 Diagnostics
• Gold Standard – Detection of IgM anti-HAV. Anti-HAV tests,
such as the enzyme immunoassay (EIA), are available
commercially.

• Polymerase Chain Reaction (PCR) – Can be used to amplify

and sequence viral genomes, particularly for outbreaks2 .
Consult with the state health department if specialized testing
(e.g., molecular testing) at CDC is warranted.
 Diagnostics
• Demonstration of viruses in feces by
immunoelectron microscopy
• Virus isolation
• Detection of antibody: ELISA
• Biochemical tests:
– ALT
– Bilirubin
– Protein
 Treatment and Prevention
• No specific therapy is available - only supportive care
• Prophylaxis with immune serum globulin given before
or early in the incubation period (i.e. < 2 weeks after
exposure)
– 80% to 90% effective in preventing clinical illness
• Active immunization with killed HAV for two doses
(initial dose + booster 6-12 months later)
• Given that the virus is transmitted through the fecal-
oral route, good hand hygiene—including handwashing
after using the bathroom, changing diapers, and before
preparing or eating food—is integral to hepatitis A
prevention
 Hepatitis A Vaccination
• The Advisory Committee on Immunization
Practices (ACIP) recommends that the
following persons be vaccinated against
hepatitis A:
– All children at age 1 year,
– Persons who are at increased risk for infection,
– Persons who are at increased risk for
complications from hepatitis A, and
– Any person wishing to obtain immunity
(protection).
 Children
• ACIP recommends that all children in the United
States receive hepatitis A vaccine at 1 year of age
(i.e., 12-23 months) to avoid interference by
passive maternal anti-HAV that may be present
during the first year of life. In the United States,
children who are not vaccinated by 2 years of age
can be vaccinated at subsequent visits;
vaccination can be considered for children 2 to 18
years old and for anyone who wants protection
against hepatitis A infection. Booster doses are
not recommended.
 Persons at Increased Risk for Hepatitis
A Infection
• Persons traveling to or working in countries that have high or intermediate
endemicity of hepatitis A. Persons who travel to developing countries are at high
risk for hepatitis A, even those traveling to urban areas, staying in luxury hotels,
and those who report maintaining good hand hygiene and being careful about
what they drink and eat.
• Men who have sex with men. Men who have sex with men should be vaccinated.
• Users of injection and non-injection drugs. Persons who use injection and non-
injection drugs should be vaccinated.
• Persons who have occupational risk for infection. Persons who work with HAV-
infected primates or with HAV in a research laboratory setting should be
vaccinated. No other groups have been shown to be at increased risk for HAV
infection because of occupational exposure.
• Persons who have chronic liver disease. Persons with chronic liver disease who
have never had hepatitis A should be vaccinated, as they have a higher likelihood
of having fulminant hepatitis A (i.e., rapid onset of liver failure, often leading to
death). Persons who are either awaiting or have received liver transplants also
should be vaccinated.
 Persons at Increased Risk for Hepatitis
A Infection
• Persons who have clotting-factor disorders. Persons who have never had
hepatitis A and who are administered clotting-factor concentrates,
especially solvent detergent-treated preparations, should be vaccinated.
• Household members and other close personal contacts of adopted
children newly arriving from countries with high or intermediate
hepatitis A endemicity. Previously unvaccinated persons who anticipate
close personal contact (e.g., household contact or regular babysitting)
with an international adoptee from a country of high or intermediate
endemicity during the first 60 days following arrival of the adoptee in the
United States should be vaccinated. The first dose of the 2-dose hepatitis
A vaccine series should be administered as soon as adoption is planned,
ideally 2 or more weeks before the arrival of the adoptee.
• Persons with direct contact with persons who have hepatitis A. Persons
who have been recently exposed to HAV and who have not previously
received hepatitis A vaccine should be vaccinated.