Micro J210 Atypical Bacteria

• 1. Chronic pulmonary disease-Mycobacterium TB
• 2. Borrelia Burgdorferi (lyme disease): vector born
• 3. Helicbacter pylori (peptic ulcer)

• -Human pathogens only
• -Cause chronic infections that can go unnoticed
• - Important to diagnose quickly
• -Curable with antibiotics if caught early

• -Gram positive
• -Nonmotile, aerobic bacillus has a very lipid rich cell wall.
• -They are not stained by normal grain stain but by acid-fast stain (acid-fast bacilli)
• -Chronic pulmonary disease

• -Cell wall lipids withstand phagocytic killing and cause necrosis of tissue
• -Able to stay alive in macrophages, intracellular growth
• - Lipoarabinomanna (LAM) can induce inflammation
• -Surface proteins are very immunogenic-Induce CMIR (Cell-meidated immune response)
• -Highly infectious (5-200 organisms can start the disease).

• -PG layer is bound to arabinogalactose-mycolic acid
• -Cell wall is overlaid with lipids such cord factor, sulfatides, wax D, and surface proteins.
• -Has a plasma membrane, PG layer, arabinogalactan, mannose-capped lipoarabinomannan, plasma-associated and cell wall associated protein, mycolic acid, glycolipid surface molecules

• -Granulomatous infection of the lung (TB)
• Effectiveness of bacterial elimination is in part related to the size of infection
• Localized collections of activated macrophages (granulomas) prevent further spread of the bacteria
• -Macrophages can penetrate into small granulomas (less than 3 mm) and kill all the organisms contained in them. Larger necrotic/caseous granulomas become encapsulated with fibrin that effectively protects bacteria from macrophage killing
• -Bacteria can remain dormant or reactivate later, when immunologic response wanes it.
• -Pulmonary disease called Wasting disease (malaise, weight loss, bloody sputum)

• -Lesions in the lung.
• -Form when an intracellular pathogen or its constituents cannot be totally eliminated.
• -infected macrophages are gathered in the center of the lesion surrounded by T cells

• aka Military TB
• -Hematogenous spread to multiple organs
• -High mortality
• -Caused by M. Tuberculosis

• -Highly infectious (5-200 to start disease)
• -Worldwide, 1/3 of population is infected with TB
• -Fewer than 15,000 new cases in US in 2003 (mostly AIDS patients)
• -Populations at risk: immunocompromised, HIV, drug/alcohol, homeless, exposed to disease
• -Humans are the only natural reservoir, person to person spread by infectious aerosols.

• -Skin test, Mantoux test
• -Reactivity of intradermal injection of mycobacterial antigen PPD
• -PPD is purified-protein derivative of cell wall
• -Reaction is measured in 48 hours
• - Induration of more than 15 mm is considered a positive skin test

• -Live attenuated Mycobacterium bovis: Bacillus of Calmette Guerin (BCG)
• -Not for immunocompromised patients
• -Recipients become skin test positive for TB
• -Effective

-HIV positive, patients receiving immunosuppressive therapy, recent contacts of patients with TB, patients with abnormal chest radiographs with prior TB

-Recent immigrants from high-prevalence countries, injection drug users, residents of high risk setting, elderly, patients with AIDS, homeless, health care/prison workers, high risk: chronic renal failure, diabetes, weight loss, children younger than 4 years or exposed to adults at high risk

-Persons at low risk for tuberculosis

• -Used for TB immunization
• -A cattle pathogen
• -Cause disease in zoo keepers/cattle farmers
• -Can cause pulmonary disease by consumption of contaminated milk but is destroyed by milk pasteurization.

-Microscopy and culture are sensitive and specific

• -Multiple drug regimens and prolonged treatment are required to prevent development of drug resistant strains
• -Control of disease through active surveillance, prophylactic and therapeutic intervention, and careful case monitoring
• -Some countries, TB vaccine

• -Lyme disease
• -Genus borrelia are gram negative bacilli
• -Spirochetes helps to penetrate tissue/cells
• -Cause of lyme disease
• -Borrelia burgdorfei: agent of lyme disease, leading cause of vector born disease in US
• - Transmitted by hard-shelled (Ixodes) ticks that live on rodents, deer, domestic pets, more recently recognized in 49 states.

• -bacteria can escape from blood and penetrate tissues (similar to PMN)
• -Outer surface protein (OSP) is very immunogenic and triggers inflammatory responses within tissues and causes damage right at the site

• Early manifestation stage:
• -Easy to treat
• -Incubation period of 3-30 days
• -A rash at the site of tick bite, erythema migrans (migrates out, bullseye), occurs in 80% of cases
• -Systemic symptoms of fatigue, headache, fever, chills, muscle pain, lymphadenopahty
• -Resolves in 4 weeks due to humoral immunity

• Late manifestation
• -Occurs in 80% of patients, hard to treat
• -Occurs when bacteria escape from blood to tissues and survive there but stimulate immune system which causes the damage (protein induces inflammation)
• -Occurs within few weeks to 2 years following onset of disease
• -Late stage has two phases

• -10-15% of patients and can last for days to months
• 1. neurological and cardiac symptoms: meningitis, encephalitis, peripheral nerve neuropathy, heart block, myopericarditis, congestive heart failure.
• 2. Arthalgias and arthritis: persist for months to years. Autoimmune arthritis which occurs in 89%

• Either of the following
• -Erythema migrans (5 in diameter)
• -At least one late manifestation (Musculoskeletal, nervous system, cardiovascular) and lab confirmation of infection

• At least one of the following:
• -Isolation of borrelia burgdorferi
• -Demonstration of diagnostic levels of immunoglobulin (IgM or IgG antibodies to the spirochetes)
• -significant increase in antibody titer between acute and convalescent serum samples

• -Discovered in 1993 as the cause of peptic ulcer
• -Gram negative curved bacilli with polar flagella
• -Present in stomach of many mammals including humans
• -Bacteria are highly motile and have several virulence factors
• -Can survive acid production
• -No animal reservoir, transmission by fecal-oral route

• 1. Urease: is an enzyme that catalyzes the hydrolysis of urea into CO2 and ammonia which locally raises the ph from 2 to 6-7
• 2. Adhesions: Mediate binding to host cells
• 3. Tissue damaging toxins: cause damage and inflammation of the lining of stomach which leads to peptic ulcer

• -45% of adults in US are colonized
• -Common, people in a low socioeconomic class or developing nations
• -Ubiquitous and worldwide with no seasonal incidence of disease
• -70-100% of patients with gastritis, gastric ulcers duodenal ulcers are infected
• -Associated with gastritis, gastric ulcers, gastric adenocarcinoma and gastric MALT lymphoma (Cancer)
• -Etiological agent of type B gastritis

• -Histological microscopic exam of gastric biopsy with upper endoscopy (Invasive)
• -Urea breath test relatively sensitive- Easier to test. Noninvasive
• -Antigen test is sensitive and specific, performed with stool specimens
• -Urease production uncommon in intestinal helicobacters

• -Treatment with antibiotics (recurrence problem)
• -No vaccines

• infection-weeks/months-chronic superficial gastritis
• years/decades: peptic ulcer, chronic superficial gastritis, lymphoproliterative disease, chronic atrophic gastritis- then adenocarcinoma