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Fever
• Fever may indicate the presence of a serious
illness, but usually a fever is caused by
common infections which are not serious
Fever in Children Causes
• Causes of fever include the following:
– Bacterial infections
– Viral infections
– Medications
• The causes of fever documented upon
discharge were, in order of frequency, upper
respiratory tract infection, nonspecific febrile
illness, diarrhea, urinary tract infection, viral
infection, pneumonia, herpangina, measles,
pneumococcal bacteremia and dengue fever.
Causes of fever in children with first febrile seizures: how common are human herpesvirus-6 and dengue virus infections?
Pancharoen C - Southeast Asian J Trop Med Public Health - 01-SEP-2000; 31(3): 521-3
MEDLINE®
Enteric Fever
• Aka Typhoid fever is a potentially fatal
multisystemic illness caused primarily by
Salmonella typhi
• Typhoid fever occurs worldwide, primarily in
developing nations whose sanitary conditions are
poor
• Typhoid fever is endemic in Asia, Africa, Latin
America, the Caribbean, and Oceania. Typhoid
fever infects roughly 21.6 million people and kills
an estimated 200,000 people every year.
Shigellosis
• Endemic throughout the world where it is
held responsible for some 120 million cases of
severe dysentery
• Majority occur in developing countries
• Involve children less than five years of age
Etiologic Agent
• Shigella species (eg, Shigella dysenteriae,
Shigella flexneri, Shigella sonnei, Shigella
boydii) are aerobic, nonmotile, glucosefermenting, gram-negative rods that are highly
contagious, causing diarrhea after ingestion of
as few as 180 organisms
• The serotype 1 of S. dysenteriae (Sd1) is of
particular concern due to its expression of the
Shiga toxin.
http://www.who.int/vaccine_research/diseases/diarrhoeal/en/index6.html
Transmission
• The organism is spread by fecal-oral contact;
via infected food or water; during travel; or in
long-term care facilities, day care centers, or
nursing homes.
Clinical Manifestations
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Acute bloody diarrhea
Crampy abdominal pain
Tenesmus
Passage of mucus
Fever (1-3 d after exposure)
Occasionally vomiting (35% prevalence)
Physical
– Lower abdominal tenderness
– Normal or increased bowel sounds
– Dehydration (occasional)
Pathogenesis
• Shigella invade the colonic epithelium by
transcytosis through M cells and penetration into
the epithelial cell layer by the basolateral
membrane, then spread laterally from cell-to-cell.
• The bacteria multiply in the cytoplasm and
eventually kill the host cell while moving towards
adjacent epithelial cells
• The Shiga toxin inhibits protein synthesis in
eukaryotic cells via inactivation of ribosomal RNA,
leading to cell death. The toxin is cytotoxic,
neurotoxic and enterotoxic.
Treatment
• Supportive care
• TMP-SMX recommended if organism is
suseptible.
• Quinolones or Nalidixic acid if organism is
resistant especially in developing countries.
Acute Gastroenteritis
• Inflammation of the gastrointestinal tract,
involving both the stomach and the small
intestine and resulting in acute diarrhea.
• The inflammation is caused most often by an
infection from certain viruses or less often by
bacteria, their toxins, parasites, or an adverse
reaction to something in the diet or
medication
Epidemiology
• Every year worldwide rotavirus in children under 5 causes 111
million cases of gastroenteritis and nearly half a million deaths.
• 82% of these deaths occur in the world's poorest nations.
• In 1980 gastroenteritis from all causes caused 4.6 million deaths in
children with most of these occurring in the third world.
• Age, living conditions, hygiene and cultural habits are important
factors.
• Lack of adequate safe water and sewage treatment has contributed
to the spread of infectious gastroenteritis
• The incidence in the developed world is as high as 1-2.5 cases per
child per year and is a major cause of hospitalization in this age
group.
Acute Gastroenteritis in Children
• Infections of the gastrointestinal tract caused by
bacterial, viral, or parasitic pathogens.
• Most are food borne illnesses.
• The most common manifestations are diarrhea and
vomiting, which may also be associated with
systemic features such as abdominal pain and fever.
Food Borne Illnesses
Etiology
Incubation
Signs and
symptoms
Labs
Bacillus cereus
1-6 hrs
Sudden onset severe nausea and vomitng
Diarrhea
Clinical diagnosis
Stool culture
Toxin
Identification
Clostridium
botulinun
12-72 hrs
Vomiting, diarrhea, blurred vision,
diplopia, dysphagia, and descending
muscle weakness
Stool and food
culture
EHEC
1-8 days
Severe diarrhea that is often bloody,
abdominal pain and vomiting. Usually,
little or no fever is present. More
common in children <4 yr old.
Stool culture
Food Borne Illnesses
Etiology
Signs and
symptoms
Labs
Abdominal cramps, fever, and diarrhea
Stools may contain blood and mucus.
Stool culture
Salmonella spp 1-3 days
Diarrhea, fever, abdominal cramps,
vomiting, fever, headache,
constipation, malaise, chills, and
myalgia
Stool culture
Shigella
24-48 hrs
Abdominal cramps, fever, and
Stool culture
diarrhea. Stools may contain blood and
mucus
Staph aureus
1-6 hrs
Sudden onset of severe nausea and
vomiting, abdominal cramps. Diarrhea
and fever may be present.
Clinical
diagnosis
Vibrio cholera
24-72 hrs.
Profuse watery diarrhea and vomiting,
Severe dehydration
Stool culture
ETEC
Incubation
1-3 days
Food Borne Illnesses
Etiology
Incubation
Signs and
symptoms
Labs
Hepatitis A
15-50 days
Diarrhea, dark urine, jaundice, and flu-like Increase in ALT,
symptoms, i.e., fever, headache, nausea,
billirubin,
and abdominal pain
Positive IgM and
anti–hepatitis A
antibodies.
Rotavirus
1-3 days
Vomiting, watery diarrhea, low-grade
fever. Temporary lactose intolerance may
occur.
Immunoassay
Other
(Adenovirus,
Parvovirus)
1—70 hrs
Nausea, vomiting, diarrhea, malaise,
abdominal pain, headache, fever
Serology
Immunoassay
Food Borne Illnesses
Etiology
Incubation
Enatmeoba
histolytioca
2-3 days to
1-4 weeks
Signs and
symptoms
Diarrhea (often bloody), frequent bowel
movements, lower abdominal pain
Labs
Stool
examination for
cysts
Clinical Manifestations
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Abdominal Pain
Nausea and vomiting
Diarrhea
Loss of appetite
Fever
Headaches
Abnormal flatulence
Abdominal pain
Abdominal cramps
Fainting and Weakness
Lethargic
Dehydration
Management
• The objective of treatment is to replace lost
fluids and electrolytes.
• Oral rehydration is the preferred treatment of
fluid and electrolyte losses caused by diarrhea
in children with mild to moderate
dehydration.
Management
• CDC recommends that breastfed infants continue to be
nursed
• Formula-fed infants should continue their usual
formula immediately upon rehydration with ORS in
amounts sufficient to satisfy energy and nutrient
requirements and at the usual concentration.
• Children receiving semisolid or solid foods should
continue to receive their usual diet during episodes of
diarrhea.
• The practice of withholding food is not recommended
and immediate normal feeding is encouraged.
Pharmacologic Treatment
• Antibiotics are usually not useful for
gastroenteritis.
• Antiemetic drugs may be helpful for vomiting
in children.
• The World Health Organization recommends
that infants and children receive a dietary
supplement of zinc for up to two weeks after
onset of gastroenteritis
Hepatitis A
• Major health problem in both developed and
developing countries
• The hepatitis A virus has a worldwide distribution. The
highest seropositivity is observed in adults in urban
Africa, Asia, and South America, where evidence of
past infection is nearly universal.
• Improvements in hygiene, public health policies, and
sanitation have had the greatest impact on this
disease, and vaccination and passive immunization
have successfully led to some reduction in illness in
high-risk groups.
Pathogenesis
• The hepatitis A virus is a single-stranded,
positive-sense, linear RNA enterovirus and a
member of the Picornaviridae family.
• Acquisition results almost exclusively from
ingestion although isolated cases of parenteral
transmission have been reported.
Pathogensis
• Hepatocyte uptake involves a receptor, on the
plasma membrane of the cell.
• Viral replication is believed to occur exclusively in
hepatocytes.
• After entry into the cell, viral RNA is uncoated,
and host ribosomes bind to form polysomes. Viral
proteins are synthesized, and the viral genome is
copied by a viral RNA polymerase. Assembled
virus particles are shed into the biliary tree and
excreted in the feces
Pathogenesis
• The period of greatest shedding of the
hepatitis A virus is during the anicteric
prodrome (14-21 d) of infection and
corresponds to the time when transmission is
highest.
Clinical Manifestations
• Prodrome
– Mild flulike symptoms of anorexia, nausea and vomiting, fatigue, malaise,
fever, myalgia, and mild headache.
• Icteric phase
– Dark urine appears first
– Pale stool soon follows
– Jaundice occurs in most (70-85%) adults with acute hepatitis The degree of
icterus also increases with age.
– Abdominal pain occurs in approximately 40% of patients.
– Itch (pruritus)
– Arthralgias and skin rash occurs on the lower limbs and may have a vasculitic
appearance.
• Relapsing hepatitis A
– Relapsing hepatitis A is an uncommon sequela of acute infection, is more
common in elderly persons, and is characterized by a protracted course of
symptoms of the disease and a relapse of symptoms and signs following
apparent resolution.
Treatment
• For acute cases of hepatitis A virus infection,
therapy is generally supportive, with no
specific treatment of acute uncomplicated
illness.
Amoebiasis
• Infection caused by Entamoeba histolytica.
• Amebiasis is the third leading parasitic cause
of death worldwide.
• Incidence of amebiasis is higher in developing
countries. Areas of high prevalence include
the Indian subcontinent, southern and
western Africa, the Far East, South America,
and Central America.
Transmission
• Food or drink contaminated with Entamoeba
cysts and direct fecal-oral contact are most
common means of infection
Etiology
• Two morphologically identical but genetically
distinct species commonly affect humans.
– Entamoeba dispar
– Entamoeba histolytica
• Infection is established by ingestion of
parasite cysts
Pathogenesis
• The ingestion of E histolytica cysts is followed
by excystation in the small bowel and invasion
of the colon by the trophozoites.
• Invasive disease begins with the adherence of
E histolytica to colonic mucins, epithelial cells,
and leukocytes. Adherence of the trophozoite
is mediated by a galactose-inhibitable
adherence lectin.
Pathogenesis
• After adherence, trophozoites invade the
colonic epithelium to produce the ulcerative
lesions typical of intestinal amebiasis.
• Numerous hemolysins, cytotoxic to the
intestinal mucosal cells, have been described
in E histolytica.
• An extracellular cysteine kinase causes
proteolytic destruction of the tissue,
producing flask-shaped ulcers.
• Spread of amebiasis to the liver occurs via the
portal blood.
• Trophozoites ascend the portal veins to
produce liver abscesses filled with acellular
proteinaceous debris.
Clinical Manifestations
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Asymptomatic cysts passage
Colicky abdominal pain
Diarrhea
Tenesmus
Blood stained stools with mucoid material
Fever
Treatment
• Invasive amebiasis is treated with
nitroimidazole followed by treatment with
luminal amebicide.
• Broad spectrum antibiotic may be indicated in
fulminant colitis.
• Perforation and megacolon are indications for
surgery
Patient
Acute Gastroenteritis
Clinical Manifestations
Fever (T=39⁰C)
Vomiting
Abdominal pain
Malaise
Anorexia
Weight loss
Headache
Productive cough
Colds
Abdominal Pain
Nausea
Vomiting
Diarrhea
Loss of appetite
Fever
Headaches
Abnormal flatulence
Fainting
Weakness
Lethargic
Dehydration
PE findings
Ill- looking
Well hydrated
Well nourished
Flushed skin
Globular abdomen, soft
Normoactive bowel sounds
Epigastric tenderness
No masses
(+/-) abdominal tenderness
Normal or increased bowel sounds
Dehydration
Laboratory
Patient
Shigellosis
Clinical Manifestations
Fever (T=39⁰C)
Vomiting
Abdominal pain
Malaise
Anorexia
Weight loss
Headache
Productive cough
Colds
Fever
Acute bloody diarrhea
Crampy abdominal pain
Tenesmus
Passage of mucus
Occasionally vomiting
PE findings
Ill- looking
Well hydrated
Well nourished
Flushed skin
Globular abdomen, soft
Normoactive bowel sounds
Epigastric tenderness
Lower abdominal tenderness
Normal or increased bowel sounds
Dehydration (occasional)
Laboratory
Routine stool culture
Patient
Hepatitis A
Clinical Manifestations
Fever (T=39⁰C)
Vomiting
Abdominal pain
Malaise
Anorexia
Weight loss
Headache
Productive cough
Colds
Mild flulike symptoms anorexia,
nausea and vomiting, fatigue,
malaise, Fever (usually <39.5°C),
myalgia, and mild headache.
Dark urine
Pale stool
Jaundice
Abdominal
Pruritus
Arthralgias and skin rash
PE findings
Ill- looking
Well hydrated
Well nourished
Flushed skin
Globular abdomen, soft
Normoactive bowel sounds
Epigastric tenderness
No masses
Hepatomegaly is common.
Jaundice or scleral icterus may
occur.
Fever
Laboratory
Patient
Dengue Fever
Clinical Manifestations
Fever (T=39⁰C)
Vomiting
Abdominal pain
Malaise
Anorexia
Weight loss
Headache
Productive cough
Colds
Fever
Pharyngeal inflammation
Rhinitis, and mild cough
Frontal or retro-orbital pain,
Myalgia and arthralgia
Nausea and vomiting Lymphadenopathy,
cutaneous hyperesthesia or hyperalgesia,
Taste aberrations, anorexia
Generalized, morbilliform, maculopapular rash
PE findings
Ill- looking
Well hydrated
Well nourished
Flushed skin
Globular abdomen, soft
Normoactive bowel sounds
Epigastric tenderness
No masses
Cold, clammy extremities, warm trunk,
flushed face, diaphoresis, restlessness,
irritability, and mid-epigastric pain
Hepatomegaly
Bleeding manifestations
Laboratory
Pancytopenia
Neutropenia white blood cell counts of
<2,000/mm3
Thrombocytopenia 100,000/mm3
hemoconcentration,
with an increase of >20% in hematocrit,
thrombocytopenia, prolonged bleeding time,
and moderately decreased prothrombin level
that is seldom <40% of control. Fibrinogen
levels may be subnormal and fibrin split
Clinical Manifestations
PE findings
Laboratory
Patient
Amoebiasis
Fever (T=39⁰C)
Vomiting
Abdominal pain
Malaise
Anorexia
Weight loss
Headache
Productive cough
Colds
Asymptomatic cysts pasaage
Colicky abdominal pain
Diarrhea
Tenesmus
Blood stained stools with mucoid
material
Fever
*Constitutional symptoms are
Ill- looking
Well hydrated
Well nourished
Flushed skin
Globular abdomen, soft
Normoactive bowel sounds
Epigastric tenderness
No masses
characteristically absent
Patient
Age group
Enteric Fever
6 year old
male
Etiologic agent
Salmonella spp.
Transmission
Fecal oral route
Signs and
Symptoms
Laboratory
findings
Fever
Cough
Colds
Abdominal
pain
Malaise
Anorexia
foul, greenyellow, liquid
diarrhea (pea
soup diarrhea
Fever
diffuse abdominal pain
and tenderness
Anorexia
Malaise
Weight loss
AGE, HEPA A, DHF
Patient
Age group
6 year old
male
Etiologic agent
Transmission
Signs and
Symptoms
Laboratory
findings
Fever
Cough
Colds
Abdominal
pain
Malaise
Anorexia
foul, greenyellow, liquid
diarrhea (pea
soup diarrhea
Acute gastroenteritis
Patient
Age group
6 year old
male
Etiologic agent
Transmission
Signs and
Symptoms
Laboratory
findings
Fever
Cough
Colds
Abdominal
pain
Malaise
Anorexia
foul, greenyellow, liquid
diarrhea (pea
soup diarrhea
Hepatitis A
Patient
Age group
Dengue Fever
6 year old
male
Etiologic agent
Salmonella spp.
Transmission
Fecal oral route
Signs and
Symptoms
Laboratory
findings
Fever
Cough
Colds
Abdominal
pain
Malaise
Anorexia
foul, greenyellow, liquid
diarrhea (pea
soup diarrhea
Fever
diffuse abdominal pain
and tenderness
Anorexia
Malaise
Weight loss
Patient
Age group
Malaria
6 year old
male
Etiologic agent
Salmonella spp.
Transmission
Fecal oral route
Signs and
Symptoms
Laboratory
findings
Fever
Cough
Colds
Abdominal
pain
Malaise
Anorexia
foul, greenyellow, liquid
diarrhea (pea
soup diarrhea
Fever
diffuse abdominal pain
and tenderness
Anorexia
Malaise
Weight loss