Typhoid fever, also known as typhoid,[1] is a common worldwide illness, transmitted by the ingestion of food or

water contaminated with the feces of an infected person, which contain the bacterium Salmonella enterica
enterica, serovar Typhi.[2][3] The bacteria then perforate through the intestinal wall and are phagocytosed by
macrophages. The organism is a Gram-negative short bacillus that is motile due to its peritrichous flagella. The
bacterium grows best at 37 °C/99 °F – human body temperature.

This fever received various names, such as gastric fever, abdominal typhus, infantile remittant fever, slow fever,
nervous fever, pythogenic fever, etc. The name of " typhoid " was given by Louis in 1829, as a derivative from
typhus.

The impact of this disease falls sharply with the application of modern sanitation techniques.

Signs 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.[4]

Classically, the course of untreated typhoid fever is divided into four individual stages, each lasting approximately
one week. In the first week, there is a slowly rising temperature with relative bradycardia, malaise, headache and
cough. A bloody nose (epistaxis) is seen in a quarter of cases and abdominal pain is also possible. There is
leukopenia, a decrease in the number of circulating white blood cells, with eosinopenia and relative lymphocytosis,
a positive diazo reaction and blood cultures are positive for Salmonella typhi or paratyphi. The classic Widal test is
negative in the first week.

In the second week of the infection, the patient lies prostrate with high fever in plateau around 40 °C (104 °F) and
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. There are rhonchi in lung bases. The abdomen is
distended and painful in the right lower quadrant where borborygmi can be heard. Diarrhea can occur in this
stage: six to eight stools in a day, green with a characteristic smell, comparable to pea soup. However, constipation
is also frequent. The spleen and liver are enlarged (hepatosplenomegaly) and tender, and there is elevation of liver
transaminases. The Widal reaction is strongly positive with antiO and antiH antibodies. Blood cultures are
sometimes still positive at this stage. (The major symptom of this fever is the fever usually rises in the afternoon up
to the first and second week.)

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 septicaemia or diffuse peritonitis sets in.
 Encephalitis
 Metastatic abscesses, cholecystitis, endocarditis and osteitis

The fever is still very high and oscillates very little over 24 hours. Dehydration ensues and the patient is delirious
(typhoid state). By the end of third week the fever has started reducing this (defervescence). This carries on into
the fourth and final week.

transaminase or an aminotransferase is an enzyme that catalyzes a type of reaction between an amino acid and
an α-keto acid. To be specific, this reaction (transamination) involves removing the amino group from the amino
acid, leaving behind an α-keto acid, and transferring it to the reactant α-keto acid and converting it into an
amino acid. The enzymes are important in the production of various amino acids, and measuring the
concentrations of various transaminases in the blood is important in the diagnosing and tracking many
diseaseCause

[edit] Transmission

Flying insects feeding on feces may occasionally transfer the bacteria through poor hygiene habits and public
sanitation conditions. Public education campaigns encouraging people to wash their hands after defecating and
before handling food are an important component in controlling spread of the disease. According to statistics from
the United States Centers for Disease Control and Prevention (CDC), the chlorination of drinking water has led to
dramatic decreases in the transmission of typhoid fever in the U.S.

A person may become an asymptomatic carrier of typhoid fever, suffering no symptoms, but capable of infecting
others. According to the CDC approximately 5% of people who contract typhoid continue to carry the disease after
they recover. The most famous asymptomatic carrier was Mary Mallon (commonly known as "Typhoid Mary"), a
young cook who was responsible for infecting at least 53 people with typhoid, three of whom died from the
disease.[5] Mallon was the first apparently perfectly healthy person known to be responsible for an "epidemic".

Many carriers of typhoid were locked into an isolation ward never to be released in order to prevent further
typhoid cases. These people often deteriorated mentally, driven mad by the conditions they lived in. [6]

[edit] Heterozygous advantage

It was been hypothesized that cystic fibrosis may have risen to its present levels (1 in 1600 in UK) due to the
heterozygous advantage that it confers against typhoid fever.[7] The CFTR protein is present in both the lungs and
the intestinal epithelium, and the mutant cystic fibrosis form of the CFTR protein prevents entry of the typhoid
bacterium into the body through the intestinal epithelium. However, the heterozygous advantage hypothesis was
proposed in one review in which the author himself writes, "Although cellular/molecular evidence presently is not
available for this hypothesis, the CF mutation may be one of several mutations that have spread in European
populations because they increased resistance to infectious diseases." Since no molecular experimental evidence
has been presented in support of this theory, this theory is not accepted by the majority of the scientific
community.

Diagnosis of typhoid

Diagnosis is made by any blood, bone marrow or stool cultures and with the Widal test (demonstration of
salmonella antibodies against antigens O-somatic and H-flagellar). In epidemics and less wealthy countries, after
excluding malaria, dysentery or pneumonia, a therapeutic trial time with chloramphenicol is generally undertaken
while awaiting the results of Widal test and cultures of the blood and stool. [8]

The term "enteric fever" is a collective term that refers to typhoid and paratyphoid. [9]

Prevention

Sanitation and hygiene are the critical measures that can be taken to prevent typhoid. Typhoid does not affect
animals and therefore transmission is only from human to human. Typhoid can only spread in environments where
human feces or urine are able to come into contact with food or drinking water. Careful food preparation and
washing of hands are crucial to preventing typhoid.
A vaccine against typhoid fever was developed during World War II by Ralph Walter Graystone Wyckoff.[10] There
are two vaccines currently recommended by the World Health Organization for the prevention of typhoid:[11] these
are the live, oral Ty21a vaccine (sold as Vivotif Berna) and the injectable Typhoid polysaccharide vaccine (sold as
Typhim Vi by Sanofi Pasteur and Typherix by GlaxoSmithKline). Both are between 50% to 80% protective and are
recommended for travelers to areas where typhoid is endemic. Boosters are recommended every 5 years for the
oral vaccine and every 2 years for the injectable form. There exists an older killed whole-cell vaccine that is still
used in countries where the newer preparations are not available, but this vaccine is no longer recommended for
use, because it has a higher rate of side effects (mainly pain and inflammation at the site of the injection). [11]

Treatment

The rediscovery of oral rehydration therapy in the 1960s provided a simple way to prevent many of the deaths of
diarrheal diseases in general.
Where resistance is uncommon, the treatment of choice is a fluoroquinolone such as ciprofloxacin[9][12] otherwise, a
third-generation cephalosporin such as ceftriaxone or cefotaxime is the first choice.[13][14][15] Cefixime is a suitable
oral alternative.[16][17]

Typhoid fever in most cases is not fatal. Antibiotics, such as ampicillin, chloramphenicol, trimethoprim-
sulfamethoxazole, Amoxicillin and ciprofloxacin, have been commonly used to treat typhoid fever in developed
countries. Prompt treatment of the disease with antibiotics reduces the case-fatality rate to approximately 1%.

When untreated, typhoid fever persists for three weeks to a month. Death occurs in between 10% and 30% of
untreated cases[citation needed]. In some communities, however, case-fatality rates may reach as high as 47%. [citation needed]

Resistance

Resistance to ampicillin, chloramphenicol, trimethoprim-sulfamethoxazole and streptomycin is now common, and

these agents have not been used as first line treatment now for almost 20 years. [citation needed] Typhoid that is resistant
to these agents is known as multidrug-resistant typhoid (MDR typhoid).

Ciprofloxacin resistance is an increasing problem, especially in the Indian subcontinent and Southeast Asia. Many
centres are therefore moving away from using ciprofloxacin as first line for treating suspected typhoid originating
in South America, India, Pakistan, Bangladesh, Thailand or Vietnam. For these patients, the recommended first line
treatment is ceftriaxone. It has also been suggested Azithromycin is better at treating typhoid in resistant
populations than both fluoroquinolone drugs and ceftriaxone. [18] Azithromycin significantly reduces relapse rates
compared with ceftriaxone.

There is a separate problem with laboratory testing for reduced susceptibility to ciprofloxacin: current
recommendations are that isolates should be tested simultaneously against ciprofloxacin (CIP) and against nalidixic
acid (NAL), and that isolates that are sensitive to both CIP and NAL should be reported as "sensitive to
ciprofloxacin", but that isolates testing sensitive to CIP but not to NAL should be reported as "reduced sensitivity to
ciprofloxacin". However, an analysis of 271 isolates showed that around 18% of isolates with a reduced
susceptibility to ciprofloxacin (MIC 0.125–1.0 mg/l) would not be picked up by this method.[19] It is not certain how
this problem can be solved, because most laboratories around the world (including the West) are dependent on
disc testing and cannot test for MICs.

Hepatic Abscess

1. Causes
1. Amebiasis
2. Bacterial Infection
 1. Aerobic Gram Negative Bacteria
2. Streptococcus species
3. Staphylococcus aureus
4. Anaerobic Bacteria (Clostridium difficile)
5. Syphilis (Treponema pallidum)
6. Neisseria Gonorrhea
2. Pathophysiology
1. Sources
1. Portal vein infection
2. Systemic bacteremia
3. Ascending Cholangitis
4. Direct extension
1. Appendicitis
2. Ruptured Peptic Ulcer
3. Empyema
2. Majority of abscesses are single
3. Subacute onset over weeks
3. Symptoms
1. Fever
2. Chills
3. Nausea
4. Anorexia
5. Weight loss
6. Right Upper Quadrant Abdominal Pain (50%)
1. Pain may radiate to right shoulder
4. Signs
1. Hepatomegaly
2. Right upper quadrant tenderness
3. Jaundice
5. Labs
1. Complete Blood Count (CBC)
1. Anemia
2. Leukocytosis
2. Liver Function Test abnormalities
1. Alkaline Phosphatase increased
2. Aspartate Aminotransferase (AST) elevated
3. Alanine Aminotransferase (ALT) elevated
3. Blood Cultures (50% sensitive)
6. Radiology
1. Abdominal XRay
1. Right diaphragm elevated
2. CT Abdomen or RUQ Ultrasound
1. Fluid filled Liver masses
7. Management
1. Empiric broad spectrum triple antibiotics
1. Clindamycin or Metronidazole and
2. Aminoglycoside and
3. Consider Ampicillin
2. Focus antibiotic coverage with Blood Culture results
3. Surgery or percutaneous drainage
An abscess (Latin: abscessus) is a collection of pus (dead neutrophils) that has accumulated in a cavity
formed by the tissue in which the pus resides on the basis of an infectious process (usually caused by
bacteria or parasites) or other foreign materials (e.g., splinters, bullet wounds, or injecting needles). It is a
defensive reaction of the tissue to prevent the spread of infectious materials to other parts of the body.

The organisms or foreign materials kill the local cells, resulting in the release of cytokines. The cytokines
trigger an inflammatory response, which draws large numbers of white blood cells to the area and
increases the regional blood flow.

The final structure of the abscess is an abscess wall, or capsule, that is formed by the adjacent healthy
cells in an attempt to keep the pus from infecting neighboring structures. However, such encapsulation
tends to prevent immune cells from attacking bacteria in the pus, or from reaching the causative organism
or foreign object.

Abscesses must be differentiated from empyemas, which are accumulations of pus in a preexisting rather
than a newly formed anatomical cavity.