Bacteria Flashcards
Enteric fever
Typhoid fever - Salmonella typhi
Paratyphoid fever - Salmonella typhi A,B,C
Pathophysiology: Salmonella typhi
penetrate gut mucosa via Peyer’s patches in jejunum/distal ileum (could lead to ulceration/ perforation) –> multiply within macrophages –> enter mesenteric lymph nodes –> thoracic duct –> bloodstream –> invade reticuloendothelial system (multiply in Kupffer cells) –> reinvade blood –> gallbladder infection
Clinical features: typhoid fever
- constipation then diarrhea
- rose spots
- fever, malaise, flu-like illness
Lab Diagnosis: Salmonella typhi
- serotyping (O,H, Vi antigens)
- WIDAL test - detects rise in antibodies against H and O antigens
Checking blood, stool, urine
Treatment: Salmonella typhi
Ceftriaxone/ Ciprofloxacin
Prevention: Salmonella typhi
good hygiene, typhoid carriers excluded from food handling
Vaccination
Salmonellosis
include all salmonellas except typhi and paratyphi
- found in poultry and diary products
Salmonellosis: Pathogenesis
ingested-> absorbed to epithelial cells in small intestine –> penetrates to lamina propria layer –> multiply in lymphoid follicles –> reticuloendothelial hyperplasia –> confined to GI tract –> inflammatory response (release of prostaglandins) –> stimulates cAMP and active fluid secretion –> diarrhea
Salmonellosis: clinical manifestations
Bacteremia: blood cultures positive
Enterocolitis
-low grade fever
- nausea, headache, vomiting, diarrhea
- stool cultures positive
Salmonellosis: Treatment
no need antibiotics, just fluid and electrolyte replacement
Vibrio cholerae: Pathogenesis
ingested –> sensitive to stomach acid, some make it to intestines –> toxin production –> diarrhea
Vibrio cholerae: clinical manifestations
due to enterotoxin
- rice water stool
- marked dehydration
- metabolic acidosis
- hypokalemia
- hypovolemic shock
Vibrio cholerae: lab diagnosis
culture
Vibrio cholerae: Treatment
rehydration with fluids and electrolytes
- tetracycline MAY be given
(erythromycin in children)
Vibrio cholerae: prevention
good hygiene
clean water and food
vaccination
Vibrio parahaemolyticus
consumption of uncooked seafood
pathogenesis unclear
Shigellosis: pathogenesis
fecal- oral route, limited to GI tract
invades mucosal epithelial cells -> multiplies and spreads within epithelial cell cytoplasm–> microabscesses leading to necrosis –> ulceration, bleeding
heat labile exotoxin affects gut and central nervous system
Shigellosis: clinical manifestations
due to exotoxin:
- abdominal pain, fever, watery diarrhea
- number of stool increases, contains mucus and blood (dysentery)
- tenesmus (Rectal spasms)
Shigellosis: treatment and prevention
mild: only symptomatic treatment
sever: ciprofloxacin
Prevention: good hygiene, no handling food until negative
Clostridium difficile: Pathogenesis
pseudomembranous colitis
-usually caused by disruption to normal gut flora (e.g. antibiotics)
Toxin A (enterotoxin) – binds to brush border membranes of gut receptor sites
Toxin B (cytotoxin_
Clostridium difficile: Clinical manifestations
- watery/bloody diarrhea
- abdominal pain
- low grade fever
- leukocytosis
- plaques and microabscesses (endoscopic findings)
- biopsy -> inflammation in lymphoid tissue, mucosa (destruction and inflammation exudates produce thick pseudomembrane)
Clostridium difficile: lab diagnosis
feces:
- cycloserine cefotixin fructose agar (CCFA)
+ detection of toxins in feces
histological changes on affected colonic mucosa
Clostridium difficile: Treatment
metronidazole/ oral vancomycin –> discontinue offending antibiotic initially
Campylobacter: pathogenesis
- unpasteurised milk, untreated water
killed in stomach, but may be protected in milk —> invade epithelium of small intestine –> inflammation –> red, white blood cells in stool
enterotoxin produced causes fluid accumulation in ileal loops
Campylobacter: clinical manifestations and treatment
- abdominal pain, bloody diarrhea, headache, malaise, fever
usually resolves without antibiotic therapy: erythromycin sensitive
Campylobacter: lab diagnosis
feces:
- -ve “sea gull wing” shape organism
- grows on skirrow’s medium
oxidase positive
Campylobater: treatment and prevention
erythromycin, ciprofloxacin
prevention: good hygiene, public health measures for milk
Helicobacter pylori: pathogenesis
chronic gastritis
peptic ulcer
mucosa-associated lymphoid tissue lymphoma (MALT)
gastric carcinoma
- grows optimally at pH 6-7, found in mucus layer near epithelial surface
- produces protease that modifies gastric mucus, reducing ability of HCl to diffuse through mucus
- potent urease acitivty–> yields production of ammonia (alkaline
- motile in mucus
Helicobacter pylori: clinical manifestations
nausea, pain, vomiting, fever
organism: spiral shaped, gram -ve
Helicobacter pylori: diagnosis
Urea breath test:
- patient swallows urea orally, broken down by urease in stomach, measures CO2
Biopsy:
rapid urease test
histology
Skirrow’s medium culture
Helicobacter pylori: Treatment
Triple therapy
proton pump inhibitor + clarithromycin + amoxicillin + (bismuth compound)
Escherichia coli: EPEC pathogenesis
- belongs to O serotypes
- attaches to epithelial cells, disrupts microvillus causing diarrhea
Eshcerichia coli: ETEC pathogenesis
- fimbrial adhesions
- enterotoxins: heat labile, heat stable
- commonly causes traveler’s diarrhea
Escherichia coli: EHEC pathogenesis
- serotype O157:H7
- produces verotoxin, binds to verotoxin receptors on renal epithelium
- causes haemorrhagic colitis (destruction of mucosa)
- causes haemorrhagic uremic syndrome
Escherichia coli: EIEC
- tissue destruction, inflammation, necrosis, ulceration, blood and mucus in stools
- due to poor hygiene
Escherichia coli: EAEC
- produces heat labile toxin
Escherichia coli: DAEC
- produces a-haemolysin, cytotoxic necrotizing factor
Escherichia coli: Treatment and prevention
no specific antibiotic
- fluid replacement
- treat hemolytic uremic syndrome
clean water, adequate sewage disposal
