Campylobacter, Helicobacter, Bacteroides, and Mycoplasma Flashcards
1
Q
What are the morphologic features of Campylobacter?
A
- Small, motile, curved, Gram-negative rods
- Microaerophilic
- C. jejuni grows better at 42ºC than at 37ºC
- Express lipooligosaccharides (which lack the O-antigen of LPS)
- Killed when exposed to gastric acids
2
Q
What are the features of disease caused by Campylobacter?
A
- The most common cause of bacterial gastroenteritis, with C. jejuni responsible for most infections
- C. jejuni produces histologic damage to the mucosal surfaces of the jejunum and other parts of the intestine
- Presents most commonly as acute enteritis with diarrhea, fever, and severe abdominal pain
- Guillain-Barré syndrome and reactive arthritis are uncommon complications, presumably through molecular mimicry
3
Q
What is the epidemiology of Campylobacter?
A
- Zoonotic infections, with contaminated poultry as the main reservoir
- Uncommon for the disease to be transmitted by food handlers
4
Q
How is Campylobacter diagnosed?
A
Identification of isolates based on growth under selective conditions, microscopic morphology, and positive oxidase and catalase tests
5
Q
What are the morphologic features of Helicobacter?
A
- Spiral Gram-negative rods that resemble campylobacters
- Highly motile (via corkscrew motility)
- Produce an abundance of urease
- Require a complex medium in microaerophilic conditions
6
Q
What is the epidemiology of Helicobacter?
A
- Humans are the primary reservoir of H. pylori
- Colonization persists for life unless the host is specifically treated
- Transmission is most likely via the fecal–oral route
7
Q
What is the pathogenesis of H. pylori infection?
A
- H. pylori use their motility, chemotaxis, urease production, and other mechanisms to adapt to the acidic conditions of the stomach and colonize a narrow protected niche near the surface of epithelial cells
- Localized tissue damage is mediated by urease byproducts, mucinase, phospholipases, and the activity of vacuolating cytotoxin A (VacA), a protein that damages invaded cells by producing vacuoles. Cytotoxin-associated gene (cagA) interferes with the normal cytoskeletal structure of the epithelia
8
Q
What are the features of H. pylori infection?
A
- Acute-phase gastritis: a feeling of fullness, nausea, vomiting, hypochlorhydria
- Chronic gastritis, with the disease confined to the gastric antrum or involving the entire stomach
- Chronic gastritis progresses to develop peptic ulcers, commonly involving the junction between the corpus and antrum (gastric ulcer) or the proximal duodenum (duodenal ulcer)
- Chronic gastritis increases the risk of gastric cancer and MALT lymphoma
9
Q
How is Helicobacter diagnosed?
A
- Histologic examination of gastric biopsy specimens
- Polyclonal and monoclonal immunoassays for H. pylori antigens in the stool
- Urea breath test
10
Q
What are the morphologic features of Vibrio?
A
- Gram-negative, facultatively anaerobic, fermentative rods
- Characterized by a positive oxidase reaction and the presence of polar flagella
- Can grow in a broad temperature range and a broad pH range but are susceptible to stomach acids
- All Vibrio spp. require NaCl for growth, most are halophilic
- Grow in estuarine and marine environments worldwide, as well as in chitinous shellfish
11
Q
How is Vibrio cholerae subdivided into serogroups?
A
Based on the O polysaccharide of LPS
12
Q
Which serogroups of V. cholerae produce the cholera toxin?
A
- O1
- O139
13
Q
What is the epidemiology of Vibrio?
A
- Spread by contaminated water and food
- A high inoculum is required to establish infection
- Prominent in communities with poor sanitation
- 3–5 million cases occur every year
14
Q
What is the pathogenesis of cholera?
A
- The cholera toxin is a complex A-B toxin. The active portion of the A subunit is internalized and interacts with G proteins that control adenylate cyclase, increasing levels of cAMP. This leads to hypersecretion of water and electrolytes
- Toxin coregulated pilus on vibrio pathogenicity island-1: a surface binding protein for the bacteriophage CTXΦ that encodes the genes for the subunits of the cholera toxin
15
Q
What are the features of cholera?
A
- Clinical manifestations begin 2–3 days after ingestion with the abrupt onset of watery diarrhea and vomiting. Fever is rare
- The feces-streaked stool specimens become colorless and odorless, free of protein, and speckled with mucus (“rice-water” stools)
- Severe fluid and electrolyte loss can lead to dehydration, painful muscle cramps, metabolic acidosis (due to bicarbonate loss), hypokalemia, and hypovolemic shock with cardiac arrhythmia and renal failure
- Mortality rate is 70% in untreated patients but <1% in patients who receive treatment
