SALMONELLOSIS

Salmonellosis is a common and widely distributed food-borne disease that is a

global major public health problem. Salmonellae are motile, non-sporulating,
non-encapsulated, gram-negative rods that are aerobic and facultative anaerobic.
They are resistant to many physical agents but can be killed by heating. They have
2 main antigens: somatic (O) & flageller (H) antigens.

Typhoid Fever (Enteric Fever)

Et. Typhoid fever is mainly caused by Salmonella Typhi (also called Salmonella
enterica serovar Typhi). Less commonly it caused by Salmonella Paratyphi (A, B,
& C) which cause similar but less severe disease.
Epid. Typhoid fever is endemic in developing countries, especially Asia. S. Typhi is
highly adapted to infect human beings; transmission occurs after (direct or
indirect) contact with infected person (sick or chronic carrier) through ingestion
of contaminated foods or water.
Path. After ingestion, S. Typhi invade the gut mucosa through "M cells" in the
terminal ileum to the mesenteric lymphoid system, then to blood- stream via the
lymphatics. This primary bacteremia is usually asymptomatic, and blood cultures
are frequently negative at this stage. Bacteria then disseminated throughout the
body and colonize organs of the reticulo-endothelial system, where they may
replicate within macrophages, then shed back to blood, causing secondary
bacteremia, which coincides with the onset of clinical symptoms.
In addition to enteritis, S. Typhi can cause inflammation, ulceration or perforation
of the Peyer patches of terminal ileum, but more commonly they heal without
scar or stricture formation.
Predisposition to infection is depend on many factors including: surface Vi
(virulence) polysaccharide capsular antigen found in S. Typhi (which interferes
with phagocytosis), dose of inoculums, state of immunity & nutrition, HLA of the
host as well as infection with H. pylori. - 442 -
C.M. I.P. is usually 1-2 wk; the manifestations are usually not specific.
Hx. High-grade fever, malaise, generalized myalgia, anorexia, headache,
vomiting, abdominal pain, and dry cough. In children, diarrhea may be present in
the earlier stages of the illness which may be followed by constipation.
Ex. Pyrexia (rarely associated with relative bradycardia), pallor, toxicity, HSM,
coated tongue, & Rose spots (macular or maculopapular rash on the trunk).
Cx. Fortunately rarely occur with good Rx. It include:-
GIT; intestinal hemorrhage or perforation (with features of peritonitis), hepatitis
(with jaundice), & cholecystitis.
Neurologic; delirium, psychosis, ↑ ICP, acute cerebellar ataxia, chorea,
deafness, & Guillain-Barre syndrome.
Others; fatal BM necrosis, DIC, HUS, nephrotic syndrome, pyelonephritis,
meningitis, endocarditis, parotitis, orchitis, & suppurative lymphadenitis.
Inv. The Dx of typhoid fever is still clinical in the developing countries.
CBP; usually there is leukopenia (although leucocytosis may occur in young
children); thrombocytopenia may be a marker of severe disease.
Serology; The classic Widal test measures antibodies against O and H antigens
of S. Typhi but it lacks sensitivity and specificity in the endemic areas. Therefore,
now it has been replaced with Monoclonal Antibodies that directly detect S.
Typhi–specific antigens in serum or S. Typhi Vi antigen in urine.
Culture is the gold standard for Dx. Stool culture may be +ve during the I.P.,
then also become +ve after the 1st wk of illness (as well as the urine culture).
Blood culture is +ve in only ≈ half of patients during early stage of disease.
PCR.
Rx.
Mild cases can be managed as outpatient, but severe cases or those associated
with Cxs should be admitted to hospital for adequate rest, hydration, nutrition
(with a bland diet), & antipyretics e.g. acetaminophen every 4–6 hr. - 443 -
 Antibiotic therapy include: high dose Amoxicillin 75-100 mg/kg/day or
Chloramphenicol 50-75 mg/kg/day, both for 2-3 wk (unless the organisms are
resistant), or fluoroquinolone e.g. Ciprofloxacin 15 mg/kg/day for only 5-7 days.
Alternative agents include: 3rd generation cephalosporins e.g. Ceftriaxone or
Cefixime for 1-2 wk; or Azithromycin for 1 wk. (see the text for doses).
Dexamethasone can be given for severely ill patients, but must be done under
strict supervision because it may masks the signs of abdominal Cxs; initial dose is
3 mg/kg then 1 mg/kg every 6 hr for 2 days.
Note: This dose is higher than that used in meningitis.
Pg. Although there are many factors that affect prognosis, generally
uncomplicated disease is usually resolves within 2-4 wk. However, even with
antibiotic Rx, relapse may occur due to the emergence of multidrug- resistant
strains of S. Typhi, especially to amoxicillin, chloramphenicol, TMP-SMZ as well as
fluoroquinolones.
Individuals who excrete S. Typhi for ≥3 mo after infection are regarded as chronic
carriers, but the risk increases with age, thus it is low in children.
Children with Schistosomiasis can develop urinary carrier state because S. Typhi
can infect the parasite itself.
Pv. Improve sanitation by handwashing & prevention of food contamination,
chlorination of water, screening of food handlers, & tracing of chronic carrier.
There are 2 vaccines; Oral live-attenuated & IM Vi capsular polysaccharide
vaccines.

Non-Typhoidal Salmonellae
Et. There are 2 most important species of NTS; S. Enteritidis & S. Typhimurium.
Other species are less common e.g. S. dublin (cattle) & S. choleraesuis (pigs).
Epid. NTS have worldwide distribution & they are a major cause of bacterial
diarrhea at all ages. They are zoonotic diseases that mainly transmitted from
animals (animals are usually asymptomatic); also they are transmitted from
person-to-person by feco-oral route.
Path. Gastric acid inhibits multiplication of Salmonellae, thus risk factors include:
achlorhydria, buffering medications, rapid gastric emptying, or large inoculums.
Other risk factors include: neonates and young infants, immune deficiencies,
malnutrition, inflammatory bowel disease, hemolytic anemia (SCA, malaria), &
schistosomiasis.
In most NTS (e.g. S. Enteritidis), the infection does not extend beyond the lamina
propria and the local lymphatics, but some species have virulence factors which
can invade the gut epithelium causing bacteremia e.g. some strains of S.
Typhimurium, S. dublin, and S. choleraesuis (although the last 2 species usually
cause uncomplicated diarrhea which require no Rx).
C.M. Acute enteritis is the most common clinical presentation of NTS which
simulate food poisoning. I.P. ≈ 24 hr, starts as abrupt onset of nausea, vomiting,
and crampy abdominal pain followed by mild to severe watery diarrhea which
sometimes contains blood and mucus. Symptoms usually subside within 2–7 days.
Cx. Transient bacteremia may follow NTS enteritis (especially in
immuno-compramized patients) → fever, chills, and septic shock. Extraintestinal
focal infections may follow bacteremia which can affect many organs →
meningitis & osteomyelitis (especially those with SCA). NTS can also cause
reactive arthritis.
Inv.
GSE; moderate number of pus cells.
Stool culture requires selective media e.g. Macconkey, XLD, BBL, or SS agar.
Blood culture requires no selective media e.g. blood or chocolate agar. - 445 -
WBC; mild leukocytosis.
Serology e.g. latex agglutination and immunofluorescence tests.
PCR.
Rx. Patients with acute enteritis require only supportive measures e.g.
rehydration; whereas antibiotics are generally not recommended for NTS
gastroenteritis because they may suppress normal intestinal flora and prolong
the excretion of Salmonella causing a remote risk of creating chronic carrier state
(usually common in adults).
However, because the risk of bacteremia in infants <3 mo of age or patients with
immunedeficiency, especially when develop signs of bacteremia or other Cxs,
they should receive an appropriate antibiotic e.g. high dose 3rd generation
cephalosporins for at least 1 wk until culture results become available.
Note: Some strains of S. Typhimurium are resistant to 5 antibiotics: ampicillin,
chloramphenicol, streptomycin, sulfonamides, and tetracycline as well as some
isolates have also reduced susceptibility to fluoroquinolones.
Pg. Most patients are fully recovered, but some develop a chronic
carrier state especially those with biliary tract disease or cholelithiasis.
Pv. Control of the infection in animals (including judicious use of
antibiotics in their food) & adequate cooking of their meat; also improve
sanitation by handwashing with prevention of food & water contamination