Miscellaneous Bacteria Flashcards
1
Q
What are obligate intracellular bacteria?
A
Bacteria that can grow and multiply only in eukaryotic cells, not as free-living organisms
2
Q
Rickettsiaceae are a family of [size, Gram stain, shape, location]
A
Rickettsiaceae are a family of small Gram-negative coccobacilli that are obligate intracellular
Note: Rickettsiaceae do not take up gram stain well; they are visualized with Giesma stain
3
Q
How are Rickettsiaceae often transmitted?
A
Insect vectors
4
Q
What are the medically important genera within Rickettsiaceae?
A
- Rickettsia rickettsii
- Coxiella burnetii
- Ehrlichia chaffeensis
- Anaplasma phagocytophilum
5
Q
Rickettsia rickettsii are [size, Gram stain, shape, location]
A
Small Gram-negative coccobacilli that are obligate intracellular
(Does not visualize well with gram stain; use Giesma stain)
6
Q
What does Rickettsia rickettsii cause?
Where is this most common?
How is it acquired?
What is the clinical presentation?
A
Rocky Mountain spotted fever
Most common in central and mid-Atlantic states
Acquired through tick bites
Triad of fever, rash, and headache
7
Q
What are the other medically important Rickettsia?
(Besides Rickettsia rickettsii)
A
- Rickettsia typhi (murine typhus)
- Rickettsia tsutsugamushi (scrub typhus)
- Rickettsia prowazekii (epidemic typhus)
- Rickettsia akari (rickettsialpox)
8
Q
Coxiella burnetii are [size, Gram stain, shape, location]
A
Small Gram-negative coccobacilli that are obligate intracellular
(Note: Does not take up gram stain well, can also be considered “gram indeterminant”)
9
Q
What does Coxiella burnetii cause?
What is the clinical presentation?
Which animal is it found in?
How is it spread to humans?
A
Q fever
Presents as fever, pulmonary infiltrates, and NO rash
Harborbed by sheep, especially placenta and fetal membranes
Spread by aerosols during the birth of lambs or other animals and through ingestion of unpasteurized milk
10
Q
Ehrlichia chaffeensis are [size, Gram stain, shape, location]
A
Small Gram-negative coccobacilli that are obligate intracellular
11
Q
What does Ehrlichia chaffeensis cause?
How is it transmitted?
What cells does it infect?
What is the clinical presentation?
A
Ehrlichiosis
Transmitted by ticks
Infects monocytes and macrophages
Fever, headaches, myalgia, thrombocytopenia, leukopenia
12
Q
Anaplasma phagocytophilum are [size, Gram stain, shape, location]
A
Small Gram-negative coccobacilli that are obligate intracellular
13
Q
What does Anaplasma phagocytophilum cause?
How is it transmitted?
What cells does it infect?
What is the clinical presentation?
A
Anaplasmosis
Transmitted by ticks
Infects neutrophils
Fever, headaches, myalgias, thrombocytopenia, leukpoenia
14
Q
Bartonella spp. are [size, Gram stain, shape, location]
A
Bartonella spp. are tiny Gram-negative bacilli that are NOT obligate intracellular
Note: Bartonella stain poorly with gram stain; visualize w/ giemsa stain)
15
Q
Which cells do Bartonella spp. invade?
A
Endothelial cells
Erythrocytes
16
Q
Bartonella henselae are [size, Gram stain, shape, location]
A
Bartonella henselae are tiny Gram-negative bacilli that are NOT obligate intracellular
17
Q
What does Bartonella henselae infection cause?
A
- Bacillary angiomatosis (immunocompromised individuals, especially with AIDS)
- Cat scratch disease (enlargement of one or more lymph nodes following a cat scratch or bit)
18
Q
Bartonella quintana are [size, Gram stain, shape, location]
A
Bartonella quintana are tiny Gram-negative bacilli that are NOT obligate intracellular
19
Q
What does Bartonella quintana infection cause?
What is it transmitted by?
Who is usually effected?
A
Bacillary angiomatosis (immunocompromised individuals, especially those with AIDS)
Endocarditis
Transmitted by lice
Homeless individuals
20
Q
Chlamydia are [location]
A
Chlymadia are obligate intracellular
21
Q
What is the life cycle of Chlamydia spp.?
A
Extracellular elementary body (EB) which is metabolically inactive
Intracellular reticular body (RB) which is metabolically active
22
Q
Which Chlamydia bacteria are medically important?
A
Chlymadia trachomatis
Chlymadia pneumoniae
Chlymadia psittaci
23
Q
What type of disease does Chlamydia trachomatis cause?
A
Sexually transmitted diseases
24
Q
What do Chlamydia pneumoniae and Chlamydia psittaci cause?
A
Pneumonia
25
Mycoplasma are [location]
Mycoplasma are NOT obligate intracellular
26
Do Mycoplasma Gram stain? Why?
Mycoplasma do not Gram-stain because they lack cell walls
27
What is unique about Mycoplasma?
Smallest organisms that can be free-living in nature and self replicating but require a media supplemented with essential components
Mycoplasma plasma membranes contain sterols which are obtained from eukaryotic cells or growth media
No cell walls so do not Gram stain
28
What do Mycoplasma have in their plasma membranes that other bacteria lack?
Sterols (obtained from eukaryotic cells or growth media)
29
What disease does Mycoplasma pneumoniae cause?
How?
Community-acquired pneumonia ("Walking pneumonia"); Symptoms are often less severe than a chest x-ray might suggest
Tightly adheres to cilia and microvilli on the surface of the bronchial epithelium
30
What are spirochetes?
Neither rods nor cocci but bacteria with a characteristic spiral shape
31
Borrelia spp. are [shape]
Borrelia spp. are spirochetes
32
Which species of Borrelia spp. are medically important?
Borrelia burgdorferi and Borrelia recurrentis
33
Borrelia burgdorferi are [shape, transmission, disease caused]
Borrelia burgdorferi are spirochetes transmitted to humans through contact with ticks and cause Lyme disease
34
Which bacteria causes Lyme disease?
What is the classic presentation of Lyme disease?
Borrelia burgdorferi
Erythema migrans: annular rash with central clearance at site of tick bite
Occurs in three stages and may present with rash, fevers, arthralgias/arthritis, arrhythmias, or neurologic findings
35
Which bacteria causes relapsing fever?
How is it transmitted to humans?
Borrelia recurrentis
Ticks and lice
36
Treponema pallidum are [shape, disease caused]
Treponema pallidum are spirochetes that cause syphilis
37
Which bacteria causes syphilis?
What are the stages of syphilis?
Treponema pallidum
1. Primary syphilis: chancre (ulcerative lesion on genitalia)
2. Secondary sphilis: rash usually on soles and palms
3. Tertiary syphilis: may occur months to years later and has variety of manifestations
38
What are the medically important subspecies of Treponema pallidum?
Treponema pallidum subspecies pertenue causes yaws
Treponema pallidum subspecies endemicum causes bejel
Treponema pallidum subspecies carateum causes pinta
* Spirochetes
* Tropical climates
* Not sexually transmitted
* Manifest as infectious skin lesions
39
Leptospira interrogans is [metabolic, shape]
Leptospira interrogans is an aerobic spirochete
40
In which animal species does Leptospira interrogans causes infections?
How is Leptospira interrogans transmitted to humans?
Rats, cattle, dogs
Transmitted to humans after exposure to water contaminated with animal urine (through ingestion, cuts in skin, exposure of conjunctiva)
41
What is the clinical presentation of Leptospira interrogans?
**Phase 1**
* Fever, chills, headache, muscle pains as organism disseminates through bloodstream
* Symptoms resolve after a week, coincident with clearance of bacteria from bloodstream
**Phase 2**
* 1-3 days after resolution of phase 1
* recurrence of symptoms (meningitis in 15% of patients)
Tetracycline, penicillin, amoxicillin, ampicillin, and erythromycin used to treat
42
Which agents are most concerning for biological warfare?
Why?
Category A Bioterrorism Agents
* Yersinia pestis
* Bacillus anthracis
* Francisella tularensis
* Clostridium botulinum (toxin)
* Hemorrhagic fever viruses
* Smallpox
**These bacteria form spores or are contagious via aerosol inhalation (easily transmissible)**
**They can also cause very severe infections**
43
Which bacteria have reservoirs in farm animals?
*Brucella* spp.
EHEC - Enterohemorrhagic *E. coli*
* Salmonella enterica* serovar enteritidis
* Bacillus anthracis*
* Coxiella burnetii*
* Leptospira interrogans*
44
Which bacteria have reservoirs in wild animals?
(Wild FYRe)
* Francisella tularensis*
* Yersinia pestis*
* Rickettsia* spp.
45
Symptomatically, how would you distinguish between a fever caused by *Rickettsia rickettsii* and one caused by *Coxiella brunetti*?
A fever caused by *Rickettsia rickettsii* is likely to have a rash
A fever caused by *Coxiella burnettii* will **not** have a rash
46
What is the causative agent of Q fever?
*Coxiella Burnetii*
47
Which two members of the *Rickettsiaceae* family are transmitted by tick bite and likley to cause fever, headache, myalgia, throboytopenia, and leukopenia?
How would you identify the causative agent?
*Ehrlichia chaffeensis* and *Anaplasma phagocytophilum*
Note: Cannot be *Coxiella burnetii* or *Rickettsia rickettsii*; decreased platelets and WBC are unique to *E. chafeensis* and *A. phagocytophilum*
**Look at the cells that are infected**
* E. chafeensis* infects monocytes and macrophages
* A. phagocytophilum* infects neutrophils
48
Describe the gram-staining of spirochetes
Spirochetes are **technically gram-negative** due to characterisitcs of their cell walls, but **most are not visualized by gram-stain because of the structure of their cell walls**
49
Which groups are more likely to contract a *Leptospira interrogans* infecton?
People who engage in water sports
The bacteria thrive in animal urine; swimming in water that is contaminated can cause disease
50
What is the treatment for Leptospira interrogans?
Tetracycline, penicillin, amoxicillin, ampicillin
51
What is the most serious complication that can arise from *Leptospira interrogans* infection?
Meningitis (occurs in 15% of cases)
52
What are the medically relevant species of *Mycobacterium?*
* *M. tuberculosis*
* *M. leprae*
* *M. bovis*
* *M. marinum*
* *M. avium*
* *M. intracellulare*
* *M. kansaii*
* *M. abcessus*
* *M. fortiuitum*
53
Are *mycobacterium* gram positive or gram negative?
Structurally, all mycobacteria are gram positive
However, their cell envelopes have high lipid content; this prevents them from taking up gram stain and makes them highly resistant to beta-lactam antibiotics
54
How can *Mycobacteria* be visualized?
*Mycobacteria* stain acid-fast
Visualize with carbol-fucshin stain
55
*Mycobacterium tuberculosis* are [gram stain, shape, location, metabolism, relevant morphology]
*Mycobacterium tuberculosis:*
* Gram (+) structure, but does not gram stain
* Use acid-fast method
* Bacillus
* Facultative intracellular
* Obligate aerobe
* Very slow growth
56
Describe the structure of the *Mycobacteria* cell envelope
* Typical cytoplasmic membrane
* Cell wall is structurally gram positive, but has a high (60%) lipid content
* Lots of **mycholic acids** (a type of long-chain fatty acid)
57
How is *M. tuberculosis* transmitted?
Human-human transmission via respiratory droplets
58
Where in the body does *M. tuberculosis* proliferate?
Within macrophages
Typically in the lungs
* Primary infection more often affects the right lobe
* Disease is associated with cavities in the apex of the lung
59
What are the 3 stages of tuberculosis infection?
Describe each one briefly
* Exposure
* Has been near an infectious (aerosol-producing) person
* Infection
* The bacteria is in the body, but controlled by the host immune system; induces granulomatous response
* The person is not sick or infectious
* Can progress to disease or remain as a latent infection
* Disease
* Clinical signs and symptoms of tuberculosis are present
* The person is infectious
* Can result from progression of primary infection **or** conversion of a latent infection to a disease state
60
Describe a latent tuberculosis infection
*Mycobacterium tuberculosis* remains in the body, but is controlled by the host immune system
* Granulomas may form to contain the bacteria
* The bacteria survive in the necrotic centers of caseous granulomas, often in the lung
* Rupture releases bacteria, may cause disease conversion
* The host is not infectious or symptomatic
61
What kinds of cells might be found in a tuberculosis granuloma?
* Macrophages
* Giant cells
* Foamy macrophages
* Epitheliod Macrophages
* Monocytes
* Neutrophils
62
Why does the immune system form tuberculosis granulomas?
**Granulomas form to protect the host from the invading bacteria that cannot be killed by the immune system**
*
63
Describe the steps in the formation of a tuberculosis granuloma
* *M. tuberculosis* **sulfatides** prevent the fusion of the phagosome with the lysosome
* The bacteria are not killed, and they multiply inside of the macrophage, possibly bursting out and infecting other macrophages
* The macrophages know they're in trouble; **cord factor** secreted by *M. tuberculosis* acts on the macrophage to increase **TNF-alpha** secretion
* **Macrophages, monocytes, and neutrophils** are recruited the the helpless, infected macrophages
* Macrophages may become giant cells, foamy macrophages, and epithelioid macrophages
* **Lymphocytes** are recruited next; they surround the macrophages
* A **fibrous cuff** forms around the macrophage
* It is now a granuloma
* The infected macrophages at the center die, creating a **caseating granuloma**
64
What are sulfatides?
Molecules secreted by *M. tuberculosis* that prevent the formation of the phagolysosome
65
What is cord factor?
What is its role in *M.* *tuberculosis* virulence?
Cord factor is secreted by *M. tuberculosis* to **increase TNF-alpha** secretion by the macrophage
You may wonder why a bacteria would promote a host immune response; most experts are also unsure
However, the hypothesis is that **increasing TNF-alpha promotes the formation of a caseating granuloma** that basically becomes a nice protected home in which *M. tuberculosis* survive and escape from to cause active diesease if it chooses
66
Which groups are at an increased risk for reactivating a latent tuberculosis infection?
* Elderly
* Alcoholics
* Malnourished
* HIV patients
* Immunosuppressed
* Chemotherapy, immunosuppressive therapy for IBD
* People who acquired latent disease in the last 2 years
* 1/2 of all reactivations happen within 2 years of primary infection
67
Describe the clinical presentation of tuberculosis disease
In general:
* Chronic disease
* Fever
* Weight loss
* Night sweats
* Upper lobe pulmonary lesions
* **Other symptoms vary depending on pulmonary or extrapulmonary tuberculosis**
68
What are the two types of tuberculosis disease?
Pulmonary TB and Extrapulmonary TB
Note: Miliary TB is a particularly severe case of tuberculosis that is classified as **both** pulmonary and exrapulmonary; the diesease is systemic
69
Describe the clinical presentation of pulmonary tuberculosis
* Chronic, productive cough
* Sputum tinged with blood
* Fever
* Weight loss
* Night sweats
* Usually forms cavities in the apex of both lungs
* Lots of bacteria thrive here
## Footnote
**Pulmonary TB is the most common kind of TB disease**
70
Describe the clinical presentation of extrapulmonary tuberculosis
Occurs most frequently in HIV or immunosuppressed patients
* Chronic illness
* Fever
* Weight loss
* Night sweats
* May spread to...
* Lymph nodes (most frequent)
* Pleura
* Genitourinary tract
* Bones/joints
* Meninges
* Peritoneum (Rare)
71
What is Pott's disease?
Tuberculosis that has spread to the spine
- Arthritis of intervertebral joints
- Damage to soft tissue
72
If tuberculosis has spread to the CNS, what are you likely to see?
Meningitis
Tuberculoma (brain abscess)
73
Describe the clinical presentation of miliary tuberculosis
Classified as **both** pulmonary and extrapulmonary
* May follow primary infection or reactivation
* Very severe; the host is basically not responding at all to the pathogen, and it **disseminates widely**
* Systemic infection
* Fever, weight loss, night sweats
* Cough may or may not be present
* Commonly causes....
* Hepatomegaly
* Splenomegaly
* Lymphadenopathy
* Miliary reticulondular (snowstorm) pattern on chest x-ray
* May also cause...
* Bone involvement
* Pott's disease (spine)
* CNS involvement
* Meningitis
* Tuberculoma (brain abscess)
74
Which groups have an increased risk of mortality from *M. tuberculosis* infection?
Groups without a long history of urbanization
Ex: Native americans, Eskimos
75
What is the histopathological signature of tuberculosis?
Granuloma
76
How is a tuberculosis infection diagnosed?
The key to diagnosis is a high degree of clinical suspicion in the correct clinical setting.
Lab tests are less reliable and may take a long time
* Tuberculin skin test
* Interferon gamma release assay (IGRA)
* Grow *M. tuberculosis* from specimen
* Acid Fast stain (AFB test)
* Nucleic acid amplification test (NAAT)
77
On two different plates with the appropriate agar, which bacteria would grow faster: *M. tuberculosis* or *M. leprae?*
* M. tuberculosis*!
* M. leprae* is obligate intracellular, and therefore cannot be cultured in the lab
78
Describe a tuberculin skin test
Often used to identify individuals with latent disease
* Purified protein derivative (PPD) of tuberculin is injected intradermally
* Re-evaluate after 48-72 hours
* Individuals with latent disease will have a **delayed-type** **hypersensitivity reaction**
* Characterized by an **induration** larger than a predetermined threshold (the threshold varies depending on your personal TB and travel history)
* Drawbacks
* Cross-reacts to produce a positive result in anywhone who has had a non-TB *Mycobacterium* infection or the BCG vaccine
* It is not very **specific**
* May be (-) during active disease
* Requires people to return to the doctor's office
79
Describe the interferon gamma release assay (IGRA)
Tests for latent tuberculosis infection
* Lymphocytes from the blood are incubated with *M. tuberculosis* antigen
* Interferon-gamma is produced if there is a latent infection
* Detect with ELISA
* Advantages
* Does not cross-react with other *Mycobacterium* or BCG vaccine
* No follow-up necessary
80
What is the "gold standard" for diagnosing a tuberculosis infection?
Grow *M. tuberculosis* from a speciment
* Old method: use **Lowenstein-Jensen** medium
* Inhibits growth of other bacteria, which allows us to (eventually) visualize the very slow-growing *M. tuberculosis*
* Need 3-6 week incubation period
* New method: use radio-labled palmitic acid agar
* Palmitic acid is metabolized by *M. tuberculosis*
* Presence of the bacteria is detected using radiolabled CO2
* This is much faster
81
Describe the AFB test
The AFB test detects Acid-Fast Bacilli; can be used to detect *M. tuberculosis*
* Stain clinical specimens using acid-fast stain
* Faster results
* Not incredibly sensitive or specific
82
Describe the Nucleic Acid Amplification Test (NAAT)
Can be used to detect *M. tuberculosis* in sputum samples to diagnose active disease
* Amplify and sequence nucleic acids using PCR
* More sensitive than AFB
83
How is *M. tuberculosis* treated?
Latent infection
* 9 months of Isoniazid
Active disease: 6 month, multi-drug regimen
* 2 months of **RIPE**
* **R**ifampin
* **I**soniazid
* **P**yrazinamide
* **E**thambutol
* Follow with 4 months of **RI******
* **R**ifampin
* **I**soniazid
84
What are the criteria for classifying a strain of *M. tuberculosis* as "Multi-Drug Resistant?"
How is it treated?
**Definition:** Resistance to both isoniazid and rifampin
**Treat with:**
* 5-6 drugs
* Direct Observation Therapy to ensure adherence
* May need surgery to reduce the bacterial load
85
What is the criteria for classifying a strain of *M. tuberculosis* as "Extensively Drug Resistant?"
Multi-drug resistant, but also resistant to quinolone and at least 1 other 2nd line tuberculosis agent
86
*Mycobacterium leprae* are [gram stain, shape, location, metabolism, relevant morphology]
* Gram (+)-like cell envelope
* But do not take up gram stain, and stain acid-fast
* Bacillus
* Obligate intracellular
* Within macrophages
* Facultative aerobe
* Grows **very slowly**
* Doubling time = 11-13 days
* Loves to grow in cooler places
* Well adapted to human host
* Lost ~1/3 of *M. tuberculosis* genes
87
Why is tuberculosis so difficult to treat with antibiotics
Several characteristics of *M. tuberculosis* make it difficult to treat
* The cell envelope is thick and rich in lipids
* Difficult for antibiotics to reach
* *M. tuberculosis* basically makes a fortress for itself inside granulomas
* Antibiotics have a hard time penetrating the granuloma to reach the bacteria
* *M. tuberculosis* grows very slowly
* Lots of time to develop resistance to drugs
88
How is *Mycobacterium leprae* transmitted?
Human-human contact
Potentially from nasal secretions (the mechanism of transmission is not well understood)
89
List the determinants of pathogenicity of *M. tuberculosis*
* **Sulfatides** prevent phagolysosome formation
* The bacteria can hang out safely in the phagosome with no degradative enzymes
* **Cord Factor** induces the macrophage to secrete TNF-alpha, which is important in the formation of granulomas
* A thick, lipid-rich (mycolic acid) **cell envelope** protects the bacteria and may alter host immunity
* *M. tuberculosis* can remain dormant in the host as a latent infection for many years (or a lifetime) and progress to active disease when the environmental conditions are optimal
90
List the determinants of pathogenicity of *Mycobacterium leprae*
* Surrounded by a dense, inert capsule
* Difficult for antibiotics to penetrate
* Slow division time
* Takes a long time to clear with antibiotic treatment
* Directly kills Schwann cells
* Causes nerve damage
91
What are the 2 major forms of leprosy?
Tuberculoid leprosy
Lepramatous leprosy ("Classic leprosy")
92
Describe the clinical presentation of tuberculoid leprosy
* Triggers an intese, cell-mediated response
* Involves Th1 (a type of helper T-cell)
* Th1 stimulates antibody production, which eventually promotes phagocytosis by macrophages
* Very few bacterium are seen in tissues
* Instead, they live in macrophages
* Causes non-caseating granuloma
* Skin legions are well-defined
* Hyperpigmented, anesthetic, macular
* Raised edges, depressed center, hairless
* Enlargement of large peripheral nerves
* May become palpabe
* Ulnar, peroneal, greater auricular
* Neuronal damage
* Muscle atrophy
* Contracture
* Loss of sensitivity
* Leads to more trauma, infection, and further damage
93
A patient presents with well-defined, non-painful skin legions. The legions are hypopigmented and macular, with raised edges and a depressed center. They are hairless.
The patient states that they have just returned from a 2-month global health trip to Indonesia.
**What is causing the skin legions?**
**How would you confirm your diagnosis?**
**How should the patient be treated?**
* The legions are most likely **Tuberculoid leprosy,** a result of *M. leprae* infection
* **Confirm diagnosis** with histologic exam and biopsy of the skin legion
* Tuberculoid leprosy will NOT have many bacteria present in the tissue
* Treat the patient with **Dapsone + Rifampin for 6-12 months**
94
Describe the clinical presentation of lepramatous leprosy ("classic leprosy")
* No cellular immune response
* Involves Th2 (a type of helper T-cell)
* Th2 helper T-cells do not release antibodies; they are more effective at clearing **extracellular bacteria;** they are basically useless against *M. leprae*, which is an intracelular pathogen
* Many bacteria are present in the tissue
* Not contained in macrophages (thanks a lot, Th2)
* Skin legions are poorly demarcated
* Can be in any shape
* Usually raised
* Usually form on cooler areas of the body
* Face, ears, wrists, elbows, butt, knees
* Leonin facies
* Thickened, folded skin of the forhead and face
* Saddle nose
* Septal perforation leading to nasal collapse
* Neuronal damage
* Decreased peripheral sensitivity
* Symmetrical in extremeties
* Leads to trauma that goes undiagnosed
* Secondary infection leads to loss of digits
95
How does *M. leprae* cause neuronal damage?
*M. leprae* kills Schwann cells directly
This leads to demyelination of peripheral neurons, which can cause nerve damage
96
How does *M. leprae* lead to the loss of appendages?
* Damage to neurons through killing of Schwann cells, demyelination
* Leads to muscle atrophy, decreased sensitivity
* This can lead to trauma that goes unnoticed
* Ex: a burn, cut or scrape
* The wound becomes infected with a secondary infection, which can cause permanent damage
* Eventually the body reabsorbs the digit or appendage?
97
How is leprosy diagnosed?
Histologic exam, biopsy of skin legion
(Cannot grow on artificial media or cell culture; obligate intracellular)
98
How is leprosy treated?
* **Tuberculoid:** Dapsone + Rifampin
* **Lepramatous:** Dapsone + Rifampin + Clofazimine
99
How can tuberculosis be prevented?
* BCG vaccine: Derived from attenuated M. Bovis
* Variable effectiveness
* Used in countries outside of USA
* Respiratiory isolation
* Prophylaxis for patients with latent TB
100
How can leprosy be prevented?
There is a low risk of transmission and progression is slow;
Examine family members and close contacts of infected individuals annually
101
Describe the clinical presentation of a *Mycobacterium bovis* infection
Presents as tuberculosis disease in humans
- This is very rare, but humans can get TB from drinking unpasteurized diairy from a cow infected with *M. bovis*
- Usually infects cows
102
Describe the clinical presentation of a *Mycobacterium marinum* disease
Causes an ulcer in soft tissue
Occurs after contact with fish, fish tanks, or salt water
103
A patient presents with an infected ulcer on his hand.
He says that he was bit by his tropical fish while he was cleaning the fish tank last weekend.
Which bacteria do you think is causing the infection?
*Mycobacterium marinum*
Infection typically occurs after contact with fish, fish tanks, or salt water
Causes an ulcer in soft tissue
104
Describe the presentation of an infection by the *M. avium-intracellulare Complex*
*M. avium-intracellulare Complex = M. avium + M. intracellulare*
* In **HIV patients**
* Bacteria are disseminated, leading to **GI disease**
* In **Elderly and Cystic Fibrosis** patients
* **Pulmonary infection**
105
Describe the clinical presentation of an *M. kansaii* infection
Pulmonary infection similar to tuberculosis
106
Describe the clinical presentation of *M. abscessus*
Rapid growth
Pulmonary infection, skin/soft tissue infection
107
Describe the clinical presentation of an *M. fortuitum* infection
Rapid growth
Pulmonary infection, skin/soft tissue infection
108
What is the difference between "*M. tuberculosis* infection" and "*M. tuberculosis* disease?"
**Infection** = there is bacteria in the body, but there are no symptoms of disease and the individual is not contagious
**Disease** = Tuberculosis, with full signs and symptoms
109
What kind of agar can be used to grow *M. tuberculosis*?
Old method: Lowenstein-Jensen medium (60% homogenized egg w/malachite green)
Newer method: Radio-labled palmitic acid agar
110
A "snow storm pattern" on chest radiography is characteristic of which disease?
Tuberculosis, especially miliary tuberculosis
111
Leonine facies and saddle nose are characteristics of which disease?
Lepramatous leprosy
112
One of your elderly, alcoholic patients is very hill;
She has a severe cough, fever, and night sweats. Her chest X-ray is shown below
**What is significant about her X-ray?**
**What is the most likely cause of your patient's infection?**
**How would you treat the infection?**
The X-ray exhibits a "snowstorm" pattern characteristic of **miliary tuberculosis**
She should be treated with 2 months of **rifampin, isoniazid, pyrazinamide, and ethambutol**, followed by 4 months of **rifampin and isoniazid** (the typical treatment for tuberculosis)
113
Is this a picture of tuberculoid leprosy or lepromatous leprosy?
How do you know?
Lepromatous; the pink marks are the acid-fast *M. leprae* taking up carbol fucshin
May bacteria are located in the tissues, a characterisitc of lepromatous leprosy
114
Is this a picture of tuberculoid leprosy or lepromatous leprosy? How do you know?
Tuberculoid
Bacteria are not present in the tissue (no bright pink patches of acid-fast bacilli)
In tuberculoid leprosy, the bacteria are engulfed by macrophages, where they are able to survive
