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PROBLEM 3

Caryn Miranda Saptari


GROUP 14
LO 1 : Salmonellosis

Salmonella Microbiology
Etiology
Small gram-negative rods (2-4 X 0.5 microns)
Most motile with flagella .
Shigella and Klebsiella are non motile.
facultative anaerobes.
Reduce nitrate.
Many genera:
Escherichia, Salmonella, Shigella, Klebsiella, Proteus,
Enterobacter, Yersinia, etc.
Some strains are opportunistic pathogens.
Some strains are true pathogens
Salmonella, Shigella, Yersinia, some strains of E. coli.
Enterobacteriaceae
Etiology
Etiology
LPS on Surface
Lipopolysaccharide
Protective outer layer of most strains
Memory immune response and antibodies
directed against LPS
Polymorphic nature of side chains is
advantageous for bacteria
Since Typhi has outer capsule, this infection is
worse.
Etiology
Antigenic components of S. Typhi
The O antigen (endotoksin, somatic antigen)
Represent side chain of repeating oligosaccharide units
projecting outwards from the LPS layer of the cell wall
The H antigen (flagellar antigen)
Occur in phase 1 and phase 2
The Vi antigen
Located in outermost layer of S.typhi
Outer membrane proteins (OMPs)
Almost half of the mass of the outer membrane is protein (porin
and non-porin proteins)
Etiology
Etiology
Overview Typhoid fever, Salmonellosis, Typhus
Enteric
Fever
Other Diarrhoeal
diseases
Paratyphoid
Fever
Non Typhoid Salmonella (NTS)
S. Paratyphi A
S. Paratyphi B / S. Schotsmuelleri
S. Paratyphi C / S. Hirschfeldii
Flea & Louse
Borne Typhus
Endemic Murine
Typhus
Epidemic Typhus
Scrub Typhus
Q Fever
Rickettsia typhi
Rickettsia prowazekii
Orientia tsutsugamushi
Typhoid Fever Salmonella typhi
Salmonellosis
Rickettsial
Diseases
Ehrlichioses & Anasplasmosis
Tick & Mite Borne Fever
Modes of Transmission
Person to person transmition
Rarely (bactery 10 - 10
6
)
Contamination of food products
Salmonella live in the chicken intestine
Contamination of food processing
contamination of process equipment food
presentation
Affecting Factor
1. Microorganisms Factor
-The number of ingested
microorganisms
-Serotypes and virulence strains

2. Host factors
-Gastric acidity
-Gastrointestinal motility
-Normal flora
-Humoral and cellular
immunization system
-Malnutrition
-Metabolic and Nutritional
Factors
-Age
-Other diseases
-Use of antibiotics
-Vaccinations
-Duration of illness

3. Environmental Factors
- Tropical and sub tropical
- Urbanization
- Standards of hygiene and
sanitation
SALMONELLOSIS
Definition
Salmonellosis is a common and widely distributed food-borne disease that
is a global major public health problem affecting millions of individuals
with significant mortality.
Salmonellae live in the intestinal tracts of warm- and cold-blooded animals
NonTyphoidal Salmonellosis
ETIOLOGY :
Salmonellae are motile, nonsporulating, nonencapsulated, gram-negative rods
that grow aerobically and are capable of facultative anaerobic growth.
They are resistant to many physical agents but can be killed by heating to
130F (54.4C) for 1 hr or 140F (60C) for 15 min.
They remain viable at ambient or reduced temperatures for days and may
survive for weeks in sewage, dried foodstuffs, pharmaceutical agents, and
fecal material.
Like other members of the family Enterobacteriaceae, Salmonella possesses
somatic O antigens and flagellar H antigens.
With the exception of a few serotypes that affect only 1 or a few animal
species, such as S. dublin in cattle and S. choleraesuis in pigs, most serotypes
have a broad host spectrum.
Typically, such strains cause gastroenteritis that is often uncomplicated and
does not need treatment, but can be severe in the young, the elderly, and
patients with weakened immunity.
The causes are typically S. Enteritidis (S. enterica serotype Enteritidis) and S.
Typhimurium (S. enterica serotype Typhimurium), the 2 most important
serotypes for salmonellosis transmitted from animals to humans

Host Factors and Conditions Predisposing to the Development of
Systemic Disease with Non-typhoidal Salmonella Strains
Neonates and young infants (3 mo of age)
HIV/AIDS
Other immune deficiencies and chronic granulomatous disease
Immunosuppressive and corticosteroid therapy
Malignancies, especially leukemia and lymphoma
Hemolytic anemia, including sickle cell disease, malaria, and
bartonellosis
Collagen vascular disease
Inflammatory bowel disease
Achlorhydria or antacid medication use
Impaired intestinal motility
Schistosomiasis, malaria
Malnutrition

Clinical Manifestation
Acute Enteritis.
The most common clinical presentation of salmonellosis is with acute
enteritis.
After an incubation period of 672 hr (mean, 24 hr), there is an abrupt onset
of nausea, vomiting, and crampy abdominal pain, primarily in the
periumbilical area and right lower quadrant, followed by mild to severe watery
diarrhea and sometimes by diarrhea containing blood and mucus.
A large proportion of children are febrile, although younger infants may
exhibit a normal or subnormal temperature.
Symptoms usually subside within 27 days in healthy children and fatalities
are rare.
However, some children develop severe disease with a septicemia-like picture
(high fever, headache, drowsiness, confusion, meningismus, seizures,
abdominal distention).
The stool typically contains a moderate number of polymorphonuclear
leukocytes and occult blood. Mild leukocytosis may be detected.
Bacteremia.
While bacteremia can occur with minimal associated symptoms in
newborns and very young infants, in older infants it typically follows
gastroenteritis and can be associated with fever, chills, and septic
shock. In patients with AIDS, recurrent septicemia appears despite
antibiotic therapy, often with a negative stool culture for Salmonella
and sometimes with no identifiable focus of infection.
Nontyphoidal Salmonella gastrointestinal infections commonly cause
bacteremia in developing countries. High rates of invasive disease with
S. Typhimurium and S. Enteritides reported from Africa (3870% of
isolates) suggest an association with HIV infections and malaria.
Extraintestinal Focal Infections.
Following bacteremia, salmonellae have the propensity to seed and
cause focal suppurative infection of many organs.
The most common focal infections involve the skeletal system,
meninges, and intravascular sites and sites of pre-existing
abnormalities; areas of bone infarction as in sickle cell disease; or
bone prostheses.
Complication
Salmonella gastroenteritis can be associated with acute dehydration and
complications resulting from delayed presentation and inadequate
treatment.
Bacteremia in younger infants and immunocompromised individuals can
have serious consequences and potentially fatal outcomes. Salmonella
organisms can seed many organ systems, leading to intracranial infections
(meningitis, focal brain abscesses) as well as osteomyelitis in children with
sickle cell disease. Reactive arthritis may follow Salmonella gastroenteritis,
usually in adolescents with HLA-B27 antigen.
In certain high-risk groups, especially those with impaired immunity, the
course of Salmonella gastroenteritis may be more complicated. Neonates,
infants <6 mo of age, and children with primary or secondary immune
deficiency may have symptoms persisting for several weeks. The course of
illness and complications may also be affected by coexisting pathologies.
In children with AIDS, the infection frequently becomes widespread
and overwhelming, causing multisystem involvement, septic shock,
and death.
In patients with inflammatory bowel disease, especially active
ulcerative colitis, Salmonella gastroenteritis may be potentially
fatal, with rapid development of toxic megacolon, bacterial
translocation, and sepsis.
In children with schistosomiasis, the Salmonella may persist and
multiply within schistosomes, leading to chronic infection unless
the schistosomiasis is effectively treated.
Prolonged or intermittent bacteremia is associated with low-grade
fever, anorexia, weight loss, diaphoresis, and myalgias, and may
occur in children with underlying problems and reticulo-endothelial
system dysfunction such as hemolytic anemia or malaria.


Diagnosis
Definitive diagnosis of Salmonella infection is based on clinical correlation of the
presentation and culturing and subsequent identification of Salmonella organisms
from feces or other body fluids.
In children with gastroenteritis, cultures of stools have higher yields than rectal
swabs.
In children with nontyphoidal Salmonella gastroenteritis, prolonged fever lasting 5
days or more and young age should be recognized as risk factors closely associated
with development of bacteremia.
In patients with sites of local suppuration, aspirated specimens should be Gram
stained and cultured.
Salmonella organisms grow well on nonselective or enriched media, such as blood
agar, chocolate agar, or nutrient broth, but stool specimens containing mixed
bacterial flora require selective media such as MacConkey, xylose-lysine-
deoxycholate (XLD), bismuth sulfite (BBL), or Salmonella-Shigella (SS) agar for
isolation.
Although other rapid diagnostic methods, such as latex agglutination and
immunofluorescence, have been developed for rapid diagnosis of Salmonella in
cultures, there are few comparable tests for rapid serologic detection. Polymerase
chain reaction (PCR) techniques may offer a rapid alternative to classic cultures but
are as yet not in widespread use in clinical settings

Identification of salmonella sp.
ORGANISM AND INDICATION DOSE AND DURATION OF TREATMENT
Salmonella infections in infants <3 mo of
age, immunocompromised persons
Cefotaxime 100200 mg/kg/day every 6 hr
for 514 days
or
Ceftriaxone 75 mg/kg/day once daily for 7
days
or
Ampicillin 100 mg/kg/day every 6 hr for 7
days
or
Chloramphenicol 15 mg/kg/day divided
every 6 hr PO for 510 days
TABLE 195-3 -- Treatment of Salmonella Gastroenteritis
Prognosis
Most healthy children with Salmonella gastroenteritis recover fully.
However, malnourished children and those who do not receive optimal supportive
treatment (are at risk for developing prolonged diarrhea and complications. Y
oung infants and immunocompromised patients often have systemic involvement,
a prolonged course, and extraintestinal foci.
In particular, children with HIV infection and Salmonella infections can have a
florid course.
After infection, nontyphoidal salmonellae are excreted in feces for a median of 5
wk.
However, after clinical recovery from Salmonella gastroenteritis, asymptomatic
fecal excretion of the organism may occur for several months, particularly in
younger children or those treated with antibiotics.
A prolonged carrier state after nontyphoidal salmonellosis is rare (<1%), but may
be seen in children with biliary tract disease and cholelithiasis following chronic
hemolysis.
Prolonged carriage of Salmonella organisms is rare in healthy children but has
been reported in those with underlying immune deficiency. During the period of
Salmonella excretion, the individual may infect others, directly by the fecal-oral
route or indirectly by contaminating foods.
Typhoid Fever
Definition of Typhoid Fever
Acute enteric infectious disease
caused by Salmonella typhi (S.Typhi).
prolonged fever, Relative bradycardia, apathetic facial
expressions, roseola, splenomegaly, hepatomegaly,
leukopenia.
intestinal perforation, intestinal hemorrhage
ETIOLOGY
Salmonella typhi
Salmonella Paratyphi A
Salmonella paratyphi B
Salmonella chloreasuis
ephidemiology
Typhoid fever as an endemic disease in
Indonesia
In 1990 9,2 per 10,000 citizen
In 1994 became 15,4 per 10,000 citizen
1981-1986 improved 35,8% : 19.596
26.606cases
Epidemiology
Fig. 1. The typhoid fever surveillance study sites
http://www.who.int/bulletin/volumes/86/4/06-039818/en/
Incidence of typhoid fever
Strongly endemic
Endemic
Sporadic cases
Characteristic Typhoid fever
PREVALENCE TYPOID FEVER
Sign and symptoms
Typhoid fever is characterized by a slowly progressive fever as
high as 40 C (104 F), profuse sweating, gastroenteritis, and
nonbloody diarrhea. Less commonly, a rash of flat, rose-
colored spots may appear.
In the first week :
a slowly rising temperature with relative bradycardia
Malaise
headache and cough
A bloody nose ( epistaxis) is seen in a quarter of cases
abdominal pain is also possible
leukopenia, with eosinopenia and relative lymphocytosis
blood cultures are positive for Salmonella typhi or paratyphi
The classic Widal test is negative in the first week.

Sign and symptoms
In the second week of the infection :
the patient lies prostrate with high fever in
plateau around 40 C (104 F)
bradycardia (sphygmothermic dissociation),
classically with a dicrotic pulse wave
Delirium is frequent, frequently calm, but
sometimes agitated. This delirium gives to
typhoid the nickname of "nervous fever
Rose spots appear on the lower chest and
abdomen in
around a third of patients
The abdomen is distended and painful in the
right lower quadrant


There are rhonchi in lung bases
Diarrhea can occur in this
stage: six to eight stools in a
day, green with a characteristic
smell, comparable to pea soup
constipation is also frequent
The spleen and liver are
enlarged (hepatosplenomegaly)
and tender
The Widal reaction is strongly
positive with anti O
and anti H antibodies
Blood cultures are sometimes
still positive at this stage. (The
major symptom of this fever is
the feve r usually rises in the
afternoon up to the first and
second week.)


Sign and symptoms
In the third week of typhoid fever, a number of complications
can occur:
Intestinal hemorrhage due to bleeding in congested
Peyer's patches; this can be very serious but is usually not
fatal.
Intestinal perforation in the distal ileum, this is a very
serious complication and is frequently fatal. It may occur
without alarming symptoms until septicemia or diffuse
peritonitis sets in.
Encephalitis
Metastatic abscesses
Cholecystitis
Endocarditis
osteitis

Sign and symptoms
The fourth week :
The fever has started reducing (defervescence
stage)
Fever come down, gradual improvement in all
symptoms and signs, but still danger

The fifth week :
convalescence stage
disappearance of all symptoms, but can relapse
Pathophysiology
patogene
Contaminated
Food
Stomach
destroyed
by HCl
pass into
the
intestine
reproduction
Penetrate to
epithelial
cells (M cell)
IgA <<<
Lamina
propria
phagocyt by
macrophages
multiply in
macrophages
Peyeri plaque
ileum distal
Mesenterica
lymph nodes
Duct.
thoracicus
blood
circulation
Bakterimia 1
(asimptomatik)
RES organ
(hepar, spleen)
left phagocytes
Multiply in the
extracellular
organ/sinusoid
blood
circulation
Bakterimia 2
(simptomatik)
Hepar
gall
bladder
intestinal
lumen
Faeces
activated
macrophages
Hyperactive
hyperplasia reaction
plaque peyeri
process
continues
erosion of blood vessels
Necrotic
hyperplasia
penetrate the mucosa
and muscle layer
Perforation
Release cytocin
& infl rx
penetrate
the gut again
delayed type hypersensitivity
reaction
Clinical forms
Mild infection:
very common seen recently
symptom and signs mild
good general condition
temperature is 38
0
C
short period of diseases
recovery expected in 1~3 weeks
young children mild more
Clinical forms
Persistent infection:
diseases continue than 5 weeks
Ambulatory infection:
mild symptoms,early intestinal bleeding or
perforation.
Clinical forms
Fulminate infection:
rapid onset
severe toxemia
Septicemia
High fever
Chill
circulation failure

Shock
Delirium
Coma
Myocarditis
bleeding
Major findings in lower ileum
Hyperplasia stage(1st week):
swelling lymphoid tissue and proliferation of macrophages.
Necrosis stage(2nd week):
necrosis of swelling lymph nodes or solitary follicles.
Ulceration stage(3rd week):
shedding of necrosis tissue and formation of ulcer -----
intestinal hemorrhage, perforation .
Stage of healing (from 4th week):
healing of ulcer, no cicatrices and no contraction

Ink Mg I Mg II Mg III Mg IV
Biakan
Darah
Biakan
Feses
Tes Widal
Negatif
Positif 60 90%
Negatif
Pos / Neg
Negatif
Positif 80 % Pos 50 %
Negatif
Positif 20 % Pos 50 % Pos 80 %
MANIFESTASI KLINIK
Diagnose
LAB diagnose
Rutine check -SGOT and SGPT increase
-leukositosis (aneusinofilia and limfopenia)
- LED increase
WIDAL TEST Aglutination reaction between S. Typhii (antigen) with antibody
(aglutinin)
TUBEX test Detect antibody anti S.Typhi 09 in the serum of patient
Typhidot TEST Antibody IGM and IG G in the outer membran of salmonela typhi
IGM dipstick test Antibody IGM specific S.Typhii in the whole blood serum
Blood culture Positive if typhoid fever but can be negative too
Therapy
Non farmaco
Rest and therapy
Diet
farmaco
DOSIS ES
kloramfenikol 4x500 mg /Hari (oral/IV) Anemia aplastik
tiamfenikol 4x500 mg/Hari Anemia aplastik
klotrimoksazole 2x 2 tablet (sulfametoksazole 400 mg dan 80 mg
trimetroprim)
ampisilim 50-150 mg/KgBB
sefalosporin 3-4 gram dalam dekstrosa 100 cc diberikan jam
infus
Complication
Complication
Intestinal -Bleeding intestinal
-Perforation
Non intestinal Hepatitis tifosa
Pankreatitis tifosa
Complication hematology
Miokarditis
neuropsikiatrik
PREVENTION
Choose food processed for safety
Prepare food carefully
Keep food contact surfaces clean
Eat cooked food as soon as possible
Maintain clean hands
Steam or boil shellfish at least 10 minutes
All milk and dairy products should be pasteurized
Control fly populations
Prevention of typhoid fever
1. Avoid risky foods and drinks.
2. Get vaccinated against typhoid fever.
Remember that you will need to complete your
vaccination at least 1 week before you travel so
that the vaccine has time to take effect!!
Taking antibiotics will not prevent typhoid fever;
they only help treat it.

VACCINES
Routine typhoid vaccination is indicated for:
travelers to endemic areas,
persons with intimate exposure to a documented
S typhi carrier (e.g, household contact),
and microbiology laboratory personnel who
frequently work with S typhi

Vaccines are not approved for use children
younger than 2 years.

Typhoid Vaccines Available in the
United States
Vaccine
Name
How Given Doses
Total Time
Needed to Set
Aside For
Vaccination
Dosing interval
Minimum
Age
Booster
Needed
Every...
Ty21a
1 capsule per
oral
4 2 weeks 2 days 6 years 5 years
ViCPS
0.50 mL
Intramuscular
Injection
1 2 weeks Not applicable 2 years 2 years
Treatment of complication
3. Toxic myocarditis:
bed rest
cardiac muscle protection drugs, dexamethasone,
digoxin.
Viral infection
Such as upper respiratory tract infection.
Abrupt onset with fever, headache, leucopenia,
sore throat, cough, coryza.
No rose spots, no enlargement of liver &
spleen. The course of illness no more than 2
weeks.
Differential diagnosis depends on typical
manifestations and blood culture.

Malaria
History of exposure to malaria.
Paroxysms(often periodic) of sequential
chill,high fever and sweating.
Headache, anorexia, splenomegaly, anemia,
leukopenia
Characteristic parasites in
erythrocytes,identified in thick or thin blood
smears.

Dengue Fever
Sudden high fever day 1-3 (above 38,5
o
C), in
day 3 or day 4-5 increase but not very high
(below 38,5
o
C)
Typhoid fever enteritis Malaria Dengue fever
Caused:
Infection by
Bacteria:
Salmonella
typhi,
Salmonella
paratyphi
S. enteritidis
bioserotypes
(e.g., S.
typhimurium)

Parasite:
Plasmodium
falciparum ,
P. vivax,P.ovale,
and P.malariae
1 of the 4
serotypes of
dengue virus,
family
Flaviviridae,
genus
Flavivirus
incubation
period
10-14 days

6-48hours 10 -15 days 4-7days
symptomps Prolonged fever,
headache,
malaise and
anorexia,
constipation,
bloody diarrhea
Nausea,
vomiting,
nonbloody
diarrhea,
fever, cramps,
myalgia and
headache
flu-like illness
with fever, chills,
muscle aches,
and headache,
nausea,
vomiting,cough,
and diarrhea.
high fever,
headaches,
joint and
muscle pain,
vomiting and a
rash, pain
behind the
eyes
DIFFERENTIAL DIAGNOSIS
Paratyphoids A, B & C The laboratory is usually
required as the final authority. The paratyphoids tend
to run a milder course with profuse rose spots.
Salmonella infection and gastroenteritis
Salmonellae, the dysentery group, and staphylococci
may occasionally cause an invasive illness resembling
typhoid fever with bacteremia. Usually, however, the
gastrointestinal symptoms are more acute than the
general manifestations, and the pyrexia much lower
and of shorter duration.

DIFFERENTIAL DIAGNOSIS
Other diseases in differential diagnosis
a. Malaria This may be mistaken for typhoid in countries
where both are endemic. A history of previous attacks,
the more rapid onset in malaria, the shivering and
sweating, the high early pyrexia, the relative infrequency
of abdominal symptoms and signs, and a positive blood
slide all point to a diagnosis of malaria.

b. Influenza Influenza may also be confused with typhoid,
but is usually of much more rapid onset with high
temperature, severe sore throat, cough, and the absence of
a palpable spleen and rose spots.

DIFFERENTIAL DIAGNOSIS
c. Bacillary dysentery This disease seldom causes much difficulty in
diagnosis. The onset is usually acute, with severe blood diarrhoea,
although in mild cases the blood may be absent. Diarrhoea with blood is
rare in early typhoid. The signs and symptoms in dysentery are usually
abdominal and remain so, the mental state and chest being clear.

d. Typhus and other rickettsial infections These conditions should be
considered important when considering the differential diagnosis. This is
because both typhus and typhoid can cause a febrile illness with delirium,
chest signs, and abdominal discomfort. In typhus, however, the onset is
acute, and the temperature high at an early stage. Shivering attacks are
common at the onset, and prostration is rapid.
The rash is quite different (brownish red in colour, and much more profuse). It
does not fade on pressure, as does the rose spot in typhoid. There is a
leucocytosis and the Weil-Felix test becomes significantly positive at about
the tenth day.

Dengue Fever
Dengue fever is virus based disease spread
by mosquitoes.
Most commonly the mosquito Aedes Aegypti.
Sign and symptomp
Criteria suspect of dengue fever
Danger signs
Character Dengue Fever
Differential Diagnose
Cause
Dengue fever is caused by any one of four
dengue viruses spread by the Aedes aegypti
mosquito.
DENGUE FEVER
Symptoms
High fever, up to 105 F (40.6 C)
A rash over most of your body, which may
subside after a couple of days and then
reappear
Severe headache, backache or both
Pain behind your eyes
Severe joint and muscle pain
Nausea and vomiting
DD - dengue fever
Risk factors
Young children and infants
Travelers coming from areas with no malaria
Pregnant women and their unborn children

MALARIA
Symptoms
Moderate to severe shaking chills
High fever
Profuse sweating as body temperature falls
Headache
Nausea
Vomiting
Diarrhea
DD malaria
Symptoms
Fatigue
Nausea and vomiting
Abdominal pain or discomfort, especially in the
area of your liver on your right side beneath your
lower ribs
Loss of appetite
Low-grade fever
Dark urine
Muscle pain
Itching
Yellowing of the skin and eyes (jaundice)
HEPATITIS A
Differential diagnose
Symptoms
Abdominal pain
Dark urine
Joint pain
Loss of appetite
Nausea and vomiting
Weakness and fatigue
Yellowing of your skin and the whites of your
eyes (jaundice)

HEPATITIS B
Differential diagnose
Symptoms
Fatigue
Fever
Nausea or poor appetite
Muscle and joint pains
Tenderness in the area of your liver

HEPATITIS C
Differential diagnose
Caused by Salmonella paratyphoid A,B,C
respectively.
in no way different from typhoid fever in
epidemiology, pathogenesis, pathology,
clinical manifestations, diagnosis, treatment
and Prophylaxis

PARATYPHOID FEVER A, B, C
Differential diagnose
Buku Ajar Infeksi & Pediatri Tropis ed.2, IDAI 2010
Harrisons Manual of Medicine 17
th
ed, McGraw Hill Companies Inc.
Disease Difference
Hepatitis Low grade fever, dark urine, jaundice. Dx: AST & ALT level
Dengue Fever Palatal vesicles, maculopapular rash, epistaxis, petechiae. Dx: blood - ELISA / PCR
Brucellosis Febrile illness similar but less severe / fever & acute monarthritis @ hip or knee (septic
arthritis) / long lasting fever & low back pain (vertebral osteomyelitis). Dx: Agglutination
assays for IgM. Difficult to distinguish from TF & early symptom of TB
TB Mostly confined in lung(s) with cough & purulent sputum production. GI TB peritonitis.
Dx: peritoneal biopsy
Malaria Febrile paroxysm at regular interval, (falcip) multiorgan dysfx.
Dx: asexual form of parasites on peripheral blood smear
Influenza Abrupt onset of systemic symptoms. Dx: tissue culture of virus from throat swab,
nasopharyngeal wash, or sputum
Tularemia
(oropharyng & GI)
Pharyngitis, cervical & mesenteric adenopathy, intestinal ulceration. Dx: microagglutination
/ tube agglutination test, PCR
Gastroenteritis Diarrhea with stools containing blood, mucus, leukocytes. Dx: blood/stool cultures
Bronchitis
Bronchopneumonia
Shigellosis w/o th/ most cases resolve in 1 week. Dx: stool culture
Systemic fungal
infections
Incidence and Timing of Various Manifestations of Untreated
Typhoid Fever
Incubation Week 1 Week 2 Week 3 Week 4 Post
Systemic Recovery
phase or
death (15%
of untreated
cases)
10%-20%
relapse; 3%-4%
chronic
carriers;
long-term
neurologic
sequelae
(extremely
rare);
gallbladder
cancer
(RR=167;
carriers)
Stepladder
fever pattern or
insidious onset
fever
Very
common
Very common
Acute high
fever
Very rare
Chills Almost all
Rigors Uncommon
Anorexia Almost all
Diaphoresis Very common
Incubation Week 1 Week 2 Week 3 Week 4 Post
Neurologic
Malaise Almost all Almost all Typhoid state
(common)
Insomnia Very
common
Confusion/de
lirium
Common Very
common
Psychosis Very rare Common
Catatonia Very rare
Frontal
headache
(usually mild)
Very
common
Meningeal
signs
Rare Rare
Parkinsonism Very rare
Ear, nose, and throat
Coated
tongue
Very
common
Sore throat
f

Incubation Week 1 Week 2 Week 3 Week 4 Post
Pulmonary
Mild cough Common
Bronchitic
cough
Common
Rales Common
Pneumonia Rare (lobar) Rare Common
(basal)
Cardiovascular
Dicrotic pulse Rare Common
Myocarditis Rare
Pericarditis Extremely
rare
g

Thrombophleb
itis
Very rare
Incubation Week 1 Week 2 Week 3 Week 4 Post
Gastrointestinal
Constipation Very common Common
Diarrhea Rare Common (pea soup)
Bloating with
tympany
Very common
(84%)


Diffuse mild
abdominal pain
Very common

Sharp right lower
quadrant pain
Rare

Gastrointestinal
hemorrhage
Very rare;
usually trace
Very common
intestinal
perforation
Rare
Hepatosplenome
galy
Common
Jaundice Common
Gallbladder pain Very rare
Incubation Week 1 Week 2 Week 3 Week 4 Post
Urogenital
Urinary
retention
Common
Hematuria Rare
Renal pain Rare
Musculoskeletal
Myalgias Very rare
Arthralgias Very rare
Rheumatologic
Arthritis (large
joint)
Extremely rare
Dermatologic
Rose spots Rare
Miscellaneous
Abscess
(anywhere)
Extremely
rare
Extremely
rare
Extremely rare
prognosis
Symptoms usually improve in 2 to 4 weeks
with treatment. The outcome is likely to be
good with early treatment, but becomes poor
if complications develop.
Symptoms may return if the treatment has not
completely cured the infection.

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