Common bacterial infections

Dr. Jamal.M.Hussein
 Gram negative
Cholera: Fluid and electrolyte lose with 24 hours
Mortality decreased from 10-0.5% with uids

● Cholera is an acute secretory diarrheal illness caused by

toxin-producing strains of the gram-negative
bacterium Vibrio cholerae.
● Severe cholera is characterized by profound fluid and
electrolyte losses in the stool and the rapid development
of hypovolemic shock, often within 24 hours from the
initial onset of vomiting and diarrhea.
● Administration of appropriate rehydration therapy
reduces the mortality of severe cholera from over 10
percent to less than 0.5 percent .
 ETIOLOGIC AGENT
V. cholerae is a diverse species and includes pathogenic and non-pathogenic variants.
Only cholera toxin-producing (toxigenic) strains of V. cholerae are associated with cholera.
V. cholerae is classified serologically; of over 200 serological groups identified, only 2 (V. cholerae O1 and
O139) have caused cholera epidemics.

200 serologic groups

Only O1 and O139 have caused epidemics
Only toxigenic strains cause cholera
 3 m cases, 100,000 deaths
Endemic in 50 countries
Contaminated food and water

EPIDEMIOLOGY:
● Cholera is vastly underreported, and precise measurements of
the morbidity and mortality attributable to V.
cholerae infection are lacking. However, there are an estimated
3 million cases of diarrheal illness and approximately 100,000
deaths worldwide caused by V. cholerae annually.
● Global distribution — Cholera primarily occurs in settings
where there is inadequate access to clean water and
sanitation.
● Cholera is endemic in approximately 50 countries.
● Transmission — V. cholerae infection is primarily acquired by
ingesting contaminated food or water .
 Asymptomatic colonization to severe diarrhea
Incubation period from a few hours up to 3-5 days

CLINICAL MANIFESTATIONS:
● Infection with V. cholerae results in a spectrum of disease,
ranging from asymptomatic intestinal colonization to
severe diarrhea .
● The clinical manifestations of cholera caused by V.
cholerae O1 versus O139 are indistinguishable.
● Incubation period — Cholera has a typical incubation
period of one to two days. However, the incubation
period of cholera varies with host susceptibility and
inoculum size and can range from several hours to as
long as three to five days.
 Mild cases -> indistinguishable
Profound and rapid electrolytes loss = severe cholera
May contain feces or bile early
Characteristic (of cholera gravis) is rice water diarrhea with ecks of mucus and shy odor.
Painless with no tenesmus.
Maximum is 10-20 ml/kg/hour.

● Diarrhea — While mild cases of V. cholerae infection may be

clinically indistinguishable from other causes of diarrheal
illness, the profound and rapid loss of fluid and electrolytes
mark severe cholera as a clinically distinct entity.
● Cholera stools may contain fecal matter and bile in the early
phases of disease . However, the characteristic symptom of
severe cholera ("cholera gravis") is the passage of profuse
"rice-water" stool, a watery stool with flecks of mucous . It
typically has a fishy odor. The diarrhea is usually painless,
without tenesmus. In children, the maximal rate of stool
excretion in severe cholera is typically between 10 and 20
ml/kg/hour . This rate of fluid loss is not typically
observed in other causes of diarrheal illness.
 High sodium, K, and HCO3
Most severe in rst 2 days and ends in 4-5 days
100% of body weight is lost in uids
Vomiting with watery emesis is common and may occur before or after diarrhea onset.
May have abdominal cramping but not severe pain that is seen in dysentery

● In addition, compared with other causes of childhood

diarrheal illness, stool from cholera patients contains a
higher concentration of sodium, as well as significant
amounts of potassium and bicarbonate
● In patients treated with proper rehydration, diarrhea is
most severe during the first two days and ends after four to
six days .The total volume loss over the course of illness
may be up to 100 percent of body weight.
● Other gastrointestinal symptoms — Vomiting, frequently
with watery emesis, is common, and may begin either
before or after the onset of diarrhea. Patients may have
abdominal cramping but typically do not have the frank
abdominal pain classically associated with dysentery.
 Clinical dx mostly
Stool culture -> isolates V. Cholera

DIAGNOSIS: Stool dipstick and dark eld microscopy can support dx if

no culture.

● Most cases of cholera are presumptively diagnosed

based on clinical suspicion in patients who present
with severe acute watery diarrhea.
● The diagnosis can be confirmed by isolation of V.
cholerae from stool cultures performed on specific
selective media.
● Rapid tests such as stool dipsticks or darkfield
microscopy can support the diagnosis in settings
where stool culture is not readily available
 Fluids
Zinc and vitamin A

TREATMENT: Abx in moderate to severe volume depletion.

Macrolides, uoroquinolones, and tetracyclines can be
used.

● Aggressive volume repletion is the mainstay of

treatment for cholera.
● Zinc and vitamine A supplimentation.
● Antibiotic therapy — Antibiotics are an adjunctive
therapy for patients with cholera and moderate to severe
volume depletion.
● The antibiotic options for cholera include macrolides,
fluoroquinolones, and tetracyclines. The choice between
them should be based on availability and local resistance
patterns.
 Oral cholera vaccine for endemic areas and areas at
risk for a cholera outbreak
PREVENTION:
● Preventing transmission — A clean water supply and
appropriate sanitation are the cornerstones of cholera
prevention. However, these can be difficult to achieve in
resource-limited settings.
● For residents in endemic areas — WHO recommends the
inclusion of oral cholera vaccines in cholera control programs
in endemic areas, in conjunction with other prevention and
control strategies .
● WHO also recommends that oral cholera vaccines be
considered as part of an integrated control program in areas at
risk for a cholera outbreak .
Enteric fever (typhoid fever)
Typhoid fever
● Its caused by salmonella typhi (gram –ve bacteria)
● Very similar and less severe disease is caused by
s.para typhi A ,B,C.
● Ratio of disease caused by s.typhi to para typhi is 10:1
Epidemiology:
● Its endemic in many developing countries.
● Incidence in developing countries range from
100-1000 cases per 100000 population.
● Ingestion of food or water contaminated with
oraganism is the most common mode of transmission
 Contaminated food and water -> terminal ileum ->
mesenteric LN -> blood (primary bacteremia)
Organs of reticuloendothelial cells -> macrophages ->

Pathogenesis: replicate -> sheds into blood again -> secondary

bacteremia -> clinical signs and symptoms

● After ingestion of contaminated food and water the

bacteria will reach terminal ileum.
● Crosses mucosa of ileum to mesenteric lymphnode
then to blood stream(primary baceremia which is
symptomless).
● Blood borne bacteria will go to organs of reticulo
endothelial system where replicate withen macrophage
then shed back to blood causing secondary bacteremia
which coincide with clinical signs and symptoms.
 Incubation 7-14 days, fever,
malaise, myalgia, headache,
anorexia, abdominal pain, diarrhea,

Clinical manifestation: constipation.

Hepatosplenomegaly
25% -> maculopapular rash (roth
spots) at 7-10th day
● Incubation period is 7-14 days.
● Range from mild fever ,malaise and dry cough to severe
illness with multiple comlication.
● Usually start with high fever ,myalgia ,headache,anorexia
and abdominal pain.
● In child diarrhea may present in earlier stage that followed
by constipation.
● Hepatospleenomegaly.
● 25% of cases there is maculopapular rash (roth spot) appear
in 7th -10th day of illness.
● Without comlication the illness will subside within 2-4
weeks
Complications:
● 1: gastrointestinal complication like perforation and hemorrhage.
● 2:central nervous system :encephalopathy psychosis, delerium,rised
intracraial pressure,meningitis ,ventriculitis deafnessand attaxia.
● 3: CVS : myocarditis ,arrhythmia, cardigenic shock and S.A node
block.
● 4: renal : HUS, pyelonephritis,nephrotis s.
● 5:pulmonary: pneumonia ,empyemia.
● 6:Bone and joint: osteomyelitis,septic arthritis
● 7:Hepatobiliary : cholecystitis,hepatitis,abscess
● 8:Hematological : hemophagocytic syndrome
Diagnosis:
● The main stay for diagnosis is blood culture or
culture of other anatomic site 40-60%.
● Stool and urine culture become +ve after 1st week.
● Leukocyte is low in relation to fever and toxicity.
● Young children have leukocytosis
● Thrombocytopenia indicates severe illness
Treatment:
● Adequate rest ,hydration and correction of electrolye
imbalance.
● Antipyretic should be given as required.
● Antibiotic therapy is critical to reduce complications.
● Cefixime ,ceftriaxone ,azithromycin and amikacin.
● Steroid is given in shock ,stupor and coma.
Prognosis:
● Prognosis depend on early diagnosis ,age and
salmonella serotype.
● Despite apropriate therapy 2-4 % relapse after initial
response to treatment.
● Individual who excrete s.typhi for more than 3
months is called chronic carrier.
Prevention:
● Central chlorination as well as domestic water
purification are important for prevention.
● Street food especially ice cream ,cut fruits are
important risk factor.
● Vaccination by oral life attenuated or polysaccharide
intramuscular vaccine for age more than 2 years .
Brucellosis:
● Human brucellosis is a zoonotic disease caused by
genus brucella that humans are accidental host aquire
illness by direct contact with animal or consumption
of animal product especially unpasteurized milk
product.
Aetiology:
● Brucella abortus (cattle)
● Brucella melitensis (goat and sheep)
● Brucella suis (swine)
● Brucella canis(dog)
Pathogenesis:
● Routes of infections include inoculation through cuts
or abrasion in the skin,cojunctival sac ,inhalation of
infected aerosole or ingestion of contaminated meat
or dairy product.
● Its obligate intracellular that lives inside monocyte
and macrophge.
● Organism that not phgocytosed by macrophage
reside within liver ,spleen,lymphnode and BM.
Clinical manifestation:
● Its systemic disease that difficult to diagnose without history of
contact with animal or food .
● Incubation is 2-4 weeks
● Acute or incidiuos
● Classical triad of fever ,arthralgia/arthritis and hepatospleenomegaly
can be demonstrated in most of cases.
● Other include abdominal pain,headache ,diarrhea, night
sweat,fatigue,vomiting,cough,pharyngitis
● Refusal to eat ,lassitude,and refusal to bear weight are common in

h
children. a state of physical or mental weariness; lack of energy.
● Neonatal and congenital infection have been described throuh
transplacental and milk.
Diagnosis:
● Thrombocytopenia,nutropenia,anemia and
pancytopenia can occur.
● Definite diagnosis is by culture of blood and bone
marrow.
● Serum agglutination test.
● igG and igM for brucella.
Treatment:
● Antipyretics
● Rehydration
● Antibiotics less than 8 years refampicin and
trimethiprime ,more than 8 years doxycycline and
refampicine for 4-6 weeks.
● For complication tripple therapy can be used.
Prevention:
● Erradication of organism from cattle, goat and sheep.
● Pasteurization of milk and dairy product.
● No vaccine available.