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After MT2 (Lectures 12-15) Flashcards

1
Q

The urethra supports colonization by some microorganisms, mainly…?

A
  • Lactobacillus
  • Staphylococcus
  • Streptococcus
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2
Q

Most of the urinary organs are anexic, meaning…?

A

They are free of microbiota.

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3
Q

Microorganisms in the urethra can rarely move into the bladder, up the ureters, and infect the __________.

A

Kidneys

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4
Q

In the male reproductive system, regions above the _________ are sterile.

A

Prostate

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5
Q

The vagina is colonized by various microorganisms, depending on ___________ levels.

A

Hormone levels

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6
Q

In the presence of estrogen, cells of the vaginal walls produce _____________.

A

Glycogen

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7
Q

In the vagina, glycogen is converted to…?

A

Lactic acid (by lactobacilli)

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8
Q

What inhibits growth of opportunistic pathogens in the vagina?

A

Acidity (pH ~4.5 due to lactobacilli)

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9
Q

One of the most common healthcare-associated infections.

A

Bacterial UTIs (urinary tract infections)

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10
Q

UTIs are more common in males or females?

A

Females

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11
Q

What are some examples of bacterial UTIs?

A
  • Infection with enteric bacteria (Escherichia coli)
  • Leptospirosis (Leptospira interrogans)
  • Streptococcal acute glomerulonephritis (Streptococcus species)
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12
Q

What are the signs and symptoms of enteric UTIs?

A
  • Frequent, urgent, and painful urination
  • Urine may be cloudy with foul odour
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13
Q

What are the pathogens/virulence factors involved in enteric UTIs?

A
  • Caused by E. coli in most cases
  • Virulence factors include flagella and attachment fimbriae
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14
Q

Describe the pathogenesis of Uropathogenic E. coli (UPEC).

A
  1. E. coli is introduced into the urethra (often in fecal contamination)
  2. E. coli adhere to epithelial cells in the urethra via fimbriae
  3. E. coli colonize epithelial cells and begin to multiply via binary fission
  4. E. coli swim up the urethra
  5. E. coli invade bladder cells and multiply within the cytosol, escaping many of the body’s defenses (cystitis)
  6. Cells of E. coli are released into the bloodstream (bacteremia)
  7. E. coli ascend to the kidneys, where they trigger inflammation (pyelonephritis)
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15
Q

Describe the epidemiology of enteric UTIs.

A
  • More common in females
  • People at risk are diabetics; nursing home patients; elderly men who have trouble emptying their bladder; patients with urinary catheters, etc.
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16
Q

Describe the diagnosis, treatment, and prevention of enteric UTIs.

A
  • Diagnosis: based on urinalysis
  • Treatment: mild cases resolve without; some treated with antimicrobials (trimethoprim & sulfamethoxazole)
  • Prevention: limiting contamination by fecal microbes
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17
Q

Zoonotic urinary disease seen primarily in animals.

A

Leptospirosis

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18
Q

What are the signs and symptoms of Leptospirosis?

A
  • Abrupt fever, myalgia, muscle stiffness, and headache
  • Rarely fatal (mortality due to kidney/liver failure, meningitis, or respiratory distress)
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19
Q

What are the pathogens/virulence factors of Leptospirosis?

A
  • Caused by Leptospira interrogans (a Spirochete)
  • Normally lives in many wild/domestic animals
  • Virulent strains make adhesins, are motile, and can evade complement activity
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20
Q

Describe the pathogenesis of Leptospirosis.

A
  1. Leptospira in urine-contaminated water enters the body through mucous membranes or skin abrasion
  2. The spirochetes infect the blood (bacteremia)
  3. Leptospira infects liver, CNS, kidneys, and other organs
  4. In most patients, the infection becomes localized in the kidneys (can be severely or fatally damaged)
  5. Patient sheds Leptospira in urine
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21
Q

Describe the epidemiology of Leptospirosis.

A
  • L. interrogans grows asymptomatically in the kidney tubules of many wild/domesticated animals
  • Transmitted to humans by contact with urine of infected animal or urine-contamined water
  • Infection occurs through breaks in the skin or mucous membranes
  • Spirochete travels via the bloodstream throughout the body
  • Occurs throughout world; at risk people include farmers, ranchers, veterinarians, butchers, etc.
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22
Q

Describe the diagnosis, treatment, and prevention of Leptospirosis.

A
  • Diagnosis: based on antibody test
  • Treatment: oral/intravenous antimicrobials
  • Prevention: avoiding contaminated water; vaccine available only for livestock/pets
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23
Q

A complication of Streptococcal respiratory disease.

A

Acute glomerulonephritis

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24
Q

Describe the pathogenesis of Streptococcal acute glomerulonephritis.

A
  1. Antibodies produced against bacterial antigens form soluble immune complexes
  2. Some immune complexes against group A streptococci strains are NOT removed from the body
  3. Immune complexes get deposited in the glomeruli of the kidneys
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25
Q

What are the signs and symptoms of Streptococcal acute glomerulonephritis?

A
  • Inflammation of the glomeruli and nephrons (glomerulonephritis)
  • Hypertension, low urine output
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26
Q

Describe the epidemiology of Streptococcal acute glomerulonephritis.

A
  • Young patients recover fully from glomerulonephritis
  • Irreversible kidney damage may occur in adults
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27
Q

What are some non-venereal diseases of the reproductive system?

A
  • Staphylococcal toxic shock syndrome
  • Bacterial vaginosis
  • Vaginal candidiasis
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28
Q

What are some venereal diseases (STDs) of the reproductive system?

A
  • Gonorrhea
  • Syphilis
  • Chlamydia
  • Genital herpes
  • Genital warts (papilloma)
  • Trichomoniasis
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29
Q

What are the signs and symptoms of toxic shock syndromes?

A
  • Sudden onset fever, chills, vomiting, diarrhea, low BP, mental confusion, and severe red rash
  • Individuals go into shock if untreated
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30
Q

What are the pathogens/virulence factors involved in toxic shock syndrome?

A
  • Caused by some strains of Staphylococcus aureus
  • Produce toxic shock syndrome toxins (TSST)
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31
Q

Describe the pathogenesis of toxic shock syndrome.

A
  • Toxemia (entry of toxins into blood) triggers toxic shock syndrome
  • TSST cause NON-specific activation of T cells; resulting in excessive cytokine production and systemic inflammation
  • Most cases occur in menstruating females
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32
Q

Why did cases of toxic shock syndromes increase in the 1980s?

A

S. aureus was found to grow exceedingly well on super-absorbent tampons.

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33
Q

What are the signs and symptoms of bacterial vaginosis?

A
  • White vaginal discharge with a “fishy” odour
  • 50% report no other symptoms
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34
Q

What pathogens cause bacterial vaginosis?

A
  • Various anaerobic bacteria
  • E.g., when normal lactobacilli are replaced by Gardnerella vaginalis & Mycoplasma hominis
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35
Q

Associated with a decline in lactobacilli numbers and pH > 4.5

A

Bacterial vaginosis

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36
Q

Bacterial vaginosis is associated with a decline in __________ numbers, and a pH greater than ___.

A
  • Decline in lactobacilli
  • pH > 4.5
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37
Q

Associated with the presence of clue cells (epithelial cells covered with bacteria).

A

Bacterial vaginosis

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38
Q

What are the signs and symptoms of vaginal candidiasis?

A
  • Severe vaginal itching and burning
  • Curd-like discharge is common
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39
Q

Describe the pathogen involved in vaginal candidiasis.

A
  • Caused by Candida albicans (normal microbiota of skin/mucous membranes)
  • Triggers infection if the vaginal pH becomes more alkaline than usual or if normal bacterial populations are reduced by antibiotics (transforms to pseudohyphal form)
  • Can become systemic in immunocompromised people (can infect tissues in essentially every body system)
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40
Q

What structure does Candida albicans take on when it becomes opportunistic?

A

Yeast form transforms into pseudohyphal form.

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41
Q

What are the signs and symptoms of gonorrhea?

A
  • Men experience painful urination and a purulent discharge
  • Women are often asymptomatic; damage to uterine tubes when try to become pregnant; some may develop pelvic inflammatory disease (PID), inflammation, fever, and abdominal pain
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42
Q

What are the pathogens/virulence factors involved in gonorrhea?

A
  • Caused by Neisseria gonorrhoeae
  • Virulence factors include fimbriae, capsule, lipooligosaccharide (endotoxin), and protease (breaks down IgA on mucous membranes)
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43
Q

Describe the pathogenesis of gonorrhea.

A
  • Bacteria attach to epithelial cells of the mucous membranes
  • Phagocytosed bacteria survive and multiply within neutrophils; spread to other parts of the body within these WBCs (rectum, pharynx, gums, etc.)
  • Babies delivered vaginally by infected mothers can become infected
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44
Q

Presence of diplococci in pus discharge is diagnostic for what STD?

A

Gonorrhea

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45
Q

What are the 4 phases of syphilis and the associated signs/symptoms?

A
  1. Primary: chancre (small, painless, reddened, hard lesion)
  2. Secondary: sore throat, headache, malaise, myalgia, lymphadenopathy, rash
  3. Latent: asymptomatic for several years
  4. Tertiary: dementia, blindness, paralysis, heart failure, or syphilitic gummas (lesion)
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46
Q

What are the pathogens/virulence factors involved in syphilis?

A
  • Caused by Treponema pallidum (a Spirochete)
  • Virulence factors have been difficult to identify (may include glycocalyx, adhesins, hyaluronidase)
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47
Q

Describe the epidemiology of syphilis.

A
  • Transmitted mostly via sexual contact; occurs worldwide (endemic among sex workers, gay sex, and users of illegal drugs)
  • Congenital syphilis (infection of the fetus) in some cases; major cause of stillbirth
  • Most individuals do NOT develop tertiary syphilis
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48
Q

_____________ is used to treat all syphilis (except tertiary).

A

Penicillin G

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49
Q

Describe the signs and symptoms of chlamydia in men and women.

A
  • Men have painful urination and pus discharge from penis
  • Women are usually asymptomatic
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50
Q

What are some diseases that chlamydial infections can cause?

A
  • Epididymitis: inflammation of the epididymis
  • Orchitis: inflammation of the testes in men
  • Pelvic
    inflammatory disease (PID): in women
  • Trachoma: disease of the eye / corneal damage (babies infected at birth;
    the leading cause of non-traumatic blindness)
  • Lymphogranuloma venereum (LGV): the formation of a
    genital lesion and bubo (painful inflamed lymph node) in the
    groin
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51
Q

The leading cause of non-traumatic blindness.

A

Trachoma (associated with chlamydial infections)

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52
Q

Describe the pathogen involved in chlamydial infections.

A
  • Caused by Chlamydia trachomatis; multiple pathogenic strains in humans; intracellular pathogen (grows within vesicles inside host cells)
  • Developmental cycle: elementary bodies (EB) are the infective form, reticulate bodies (RB) are the reproductive form
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53
Q

Describe the developmental cycle of chlamydial infections.

A
  1. EB attaches to receptor on host cell
  2. EB triggers its own endocytosis by host cell
  3. EB converts into RB within vesicle (10 hours)
  4. RB divides rapidly, resulting in multiple RBs (the vesicle is now called an inclusion body)
  5. Most RBs convert back into EBs (21 hours)
  6. EBs are released from host cell (40 hours; cycle starts all over again)
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54
Q

Describe the pathogenesis of chlamydial infections.

A
  • Microbe enters body through scrapes/cuts
  • Infect conjunctiva or cells lining mucous membranes
  • Spread to the lymphatic system, in some cases causing proctitis (inflammation of the rectum; pain, bleeding, discharge)
  • Adolescent infection increases cervical cancer risk
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55
Q

Most common cause of infectious infertility in women.

A

Chlamydia

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56
Q

Most common reportable STD in the United States.

A

Chlamydia

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57
Q

How are chlamydial infections diagnosed?

A

Detection of chlamydial DNA by PCR.

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58
Q

Small blisters on or around the genitals or rectum.

A

Genital herpes

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59
Q

What virus causes most causes of genital herpes?

A
  • Human Herpesvirus 2 (HHV-2)
  • The remainder of cases are caused by HHV-1
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60
Q

Describe the pathogenesis of genital herpes.

A
  • Herpesvirus kills epithelial cells at infection site
  • Blisters/lesions may form at sites far from initial infection
  • Virus can become latent in nerve cells
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61
Q

Most of the world’s population is estimated to be infected with…?

A

Herpesvirus 1 or 2

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62
Q

How much higher is the risk of HIV infection with genital herpes?

A

4x higher

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63
Q

Describe the epidemiology of genital herpes.

A
  • Babies can become infected during birth (infected pregnant women should deliver by C-section)
  • Circumcised males are at lower risk of infection
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64
Q

What are the signs and symptoms of genital warts?

A
  • Papillomas or warts (growths of skin epithelium)
  • May form on the face, trunk, hands, feet, elbows, knees, or genitalia (genital warts)
  • Warts range in size from almost undetectable small bumps to large cauliflower-like growths called condylomata acuminata
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65
Q

Large cauliflower-like growths associated with (genital) warts.

A

Condylomata acuminata

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66
Q

What virus is genital warts caused by?

A

Human Papillomaviruses (HPV)

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67
Q

A common STD; causes nearly all cervical cancers.

A

Genital warts

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68
Q

What are the signs and symptoms of Trichomoniasis.

A
  • Females have vaginal discharge and irritation
  • Males are typically asymptomatic
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69
Q

Describe the pathogens/virulence factors involved in Trichomoniasis.

A
  • Caused by Trichomonas vaginalis
  • Reproduces at pH 5-6
  • Various virulence factors: adhesins, proteolytic enzymes, hemolysis, and cell-detaching factors
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70
Q

Most common curable STD in women.

A

Trichomoniasis

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71
Q

Trichomoniasis increases risk of infection by ____.

A

HIV

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72
Q

FIRST PART OF LECTURE 13

A

HERE

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73
Q

What are the signs and symptoms of oral herpes?

A
  • Presence of cold sores
  • Infections may extend beyond the oral cavity (mostly in young patients and immunocompromised individuals): herpetic gingivostomatisis, pharyngitis, or esophagitis
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74
Q

Most cases of oral herpes are caused by what virus?

A

Human Herpesvirus 1 (HHV-1)

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75
Q

Describe the pathogenesis of oral herpes.

A
  • HHV-1 infects epithelial cells, triggering inflammation and cell death resulting in painful, localized lesions
  • Virions form syncytia to avoid host’s immune system
  • Latency established in the trigeminal nerve ganglion
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76
Q

Describe the epidemiology of oral herpes.

A
  • Infections occur by causal contact in childhood
  • Primary infections are usually asymptomatic
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77
Q

What are the signs and symptoms of mumps?

A
  • Parotitis: swelling of parotid salivary glands
  • Associated with pain, fever, headache, and sore throat
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78
Q

Describe the virus involved in mumps.

A
  • Mumps virus (enveloped, -ssRNA virus)
  • Virus enters via the respiratory tract and infects salivary glands
  • Can also cause inflammation of testes, meninges, or pancreas
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79
Q

How is mumps transmitted?

A
  • Humans are the only natural host
  • Spreads via direct contact and fomites contaminated with saliva from an infected person
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80
Q

What are the signs and symptoms of viral gastroenteritis?

A
  • Nausea, vomiting, diarrhea, abdominal pain, and cramps (similar to those of bacterial gastroenteritis)
  • Dehydration is common complication
  • Bloody stool and dysentery may occur
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81
Q

Describe the pathogens involved in viral gastroenteritis.

A
  • Caused by caliciviruses, astroviruses, and rotaviruses
  • Calciviruses/Astroviruses: small, naked, +ssRNA (cause acute gastroenteritis)
  • Rotaviruses: naked dsDNA viruses
  • Viruses infect cells lining the intestinal tract
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82
Q

Describe the epidemiology of viral gastroenteritis.

A
  • Disease transmission is via the fecal-oral route from contaminated food and water
  • More cases occur in winter
  • Rotaviruses are important cause of childhood deaths in developing countries (vaccine exists)
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83
Q

Important cause of childhood deaths in developing countries.

A

Rotaviruses

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84
Q

What are some tests to diagnose viral gastroenteritis?

A
  • Serological test distinguishes among viruses
  • xTAG GPP nucleic acid test can also identify some of the viruses
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85
Q

What are the signs and symptoms of viral hepatitis?

A
  • Hepatitis = inflammation of the liver
  • Jaundice, abdominal pain, fatigue, vomiting, and weight loss
  • Symptoms may occur years after initial infection
  • Complications from chronic infection: cirrhosis, liver failure, and liver cancer
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86
Q

Liver damage in viral hepatitis infection is due mostly to what?

A

Host immune response.

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87
Q

What are the 5 different viruses that cause hepatitis?

A
  1. Hepatitis A virus (HAV)
  2. Hepatitis B virus (HBV)
  3. Hepatitis C virus (HCV)
  4. Hepatitis Delta virus (HDV)
  5. Hepatitis E virus (HEV)
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88
Q

What hepatitis viruses are chronic carrier states?

A
  • HAV
  • HCV
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89
Q

What is the common name of Hepatitis A virus (HAV)?

A

Infectious hepatitis

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90
Q

What is the common name of Hepatitis B virus (HBV)?

A

Serum hepatitis

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91
Q

What is the common name of Hepatitis C virus (HCV)?

A

Chronic hepatitis

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92
Q

Does HAV cause hepatic cancer?

93
Q

What type of hepatitis virus infects millions of people worldwide?

94
Q

Vaccines are available against what types of hepatitis viruses?

A

HAV and HBV

95
Q

What are the signs and symptoms of giardiasis?

A
  • Often asymptomatic
  • Diarrhea and associated symptoms can last up to 4 weeks
96
Q

What is giardiasis caused by?

A
  • Caused by Giardia intestinalis (protozoan)
  • G. intestinalis cysts are resistant to chlorine, heat, drying, and stomach acid
97
Q

Describe the pathogenesis of giardiasis.

98
Q

Who are at particular risk for giardiasis?

A
  • Hikers
  • Campers
  • Swimmers
99
Q

What are the signs and symptoms of cryptosporidiosis?

A
  • Severe watery diarrhea lasting about 2 weeks
  • Headache, muscular pain, cramping, fatigue, severe fluid/weight loss
100
Q

What pathogen causes cryptosporidiosis?

A
  • Caused by Cryptosporidium parvum (protozoan)
  • Motile sporozoite is infectious; form tick-shelled oocysts inside cells
101
Q

What are the signs and symptoms of amebiasis?

A
  • Luminal amebiasis = asymptomatic
  • Invasive amebic dysentery = severe diarrhea, colitis, and appendicitis
  • Invasive extraintestinal amebiasis = necrotic lesions in various organs
102
Q

Describe the pathogen that causes amebiasis.

A
  • Entamoeba histolytica (protozoan)
  • Virulent strains produce numerous proteins that are toxic to cells and facilitate invasion
103
Q

Describe the pathogenesis of amebiasis.

A
  • Infection starts with the ingestion of thick-shelled cysts
  • Trophozoites are released in the intestine where they multiply and cause lumina amebiasis
  • When trophozoites invade the peritoneal cavity or blood => amebic dysentery or invasive extraintestinal amebiasis occurs
104
Q

Majority of infected individuals develop what type of amebiasis?

A

Luminal amebiasis

105
Q

__% of the world’s population are carriers for amebiasis.

106
Q

Describe tapeworms.

A
  • Scientific name = cestode
  • Flat, segmented, parasitic helminth that lack their own digestive system
  • Helminths can infest the GI tract as non-disease causing parasites
  • Life cycle split between primary and intermediate host
107
Q

What are the signs and symptoms of tapeworm infestation?

A
  • Usually asymptomatic
  • Nausea, abdominal pain, weight loss, and diarrhea may occur
108
Q

What pathogens cause tapeworm infestation?

A
  • Taenia saginata (beef tapeworm)
  • Taenia solium (pork tapeworm)
109
Q

Diagnosed by presence of proglottids in fecal sample.

A

Tapeworm infestation

110
Q

Describe the pathogenesis of tapeworm infestation.

A
  1. Eggs and egg-filled proglottids are passed into the environment in feces
  2. Intermediate hosts ingest eggs on contaminated food
  3. Eggs hatch into larvae that penetrate the intestinal wall and migrate to other tissues
  4. Larva develop into a cysticerus in muscle
  5. Humans ingests cysticerus in raw or undercooked contaminated meat
  6. Cysticerus excysts and attaches to mucosa of small intestine as a scolex, which matures
  7. Adult worm forms new proglottids
111
Q

Describe pinworms.

A
  • Pinworms are nematodes
  • Long, thin, unsegmented, cylindrical helminth
112
Q

What are the signs and symptoms of pinworm infestation?

A
  • 1/3rd of cases are asymptomatic
  • Perianal itching, irritability, and decreased appetite
113
Q

Describe the pathogen that causes pinworm infestation.

A
  • Caused by Enterobius vermicularis
  • Females deposit eggs in the perianal region at night; eggs can be dislodged and spread the disease
114
Q

The most common parasitic worm in the US.

A

Enterobius

115
Q

Results from infestation by several parasitic nematodes.

A

Anisakiasis

116
Q

What are the signs and symptoms of anisakiasis?

A
  • Typically asymptomatic
  • Abdominal pain, nausea, vomiting, and fever may occur
  • Some individuals develop an allergic rash (IgE-mediated allergic reaction)
117
Q

Describe the pathogen that causes anisakiasis.

A
  • Caused by Anisakis simplex (parasite of marine animals)
  • Complex life cycle with several large stages
  • Transmitted to humans in raw or undercooked fish
118
Q

About 20,000 cases are estimated to occur worldwide of this disease.

A

Anisakiasis

119
Q

Describe the pathogenesis of anisakiasis.

A
  1. Marine mammals excrete eggs
  2. Two larval stages develop inside eggs
  3. Eggs hatch, and larvae swim freely
  4. Krill eat larvae
  5. Fish eat krill
  6. Fish eat fish
  7. Marine mammals eat infected fish (larvae mature, mate, and lay eggs in intestine)
  8. Humans eat infected, raw, or undercooked fish and become accidental hosts
120
Q

What is the central nervous system (CNS) composed of?

A
  • Brain
  • Spinal cord
121
Q

Nerves transfer commands from CNS to muscles and glands.

A

Peripheral nervous system (PNS)

122
Q

What types of cranial and spinal nerves make up the PNS?

A
  • Sensory nerves
  • Motor nerves
  • Mixed nerves
123
Q

CNS has NO normal microbiota, meaning it is an _________ environment.

124
Q

What ways can pathogens access the CNS?

A
  • Breaks in the bones and meninges (protective layers of membrane that surround and shield the brain and spinal cord)
  • Medical procedures
  • Travel via axonal transport in peripheral neurons to CNS
  • By infecting and killing cells of the meninges (meningitis)
  • Inflammation can alter the permeability of the blood-brain barrier
125
Q

Protective layers of membrane that surround and shield the brain and spinal cord.

126
Q

Bacteria can infect cells of the nervous system… examples include:

A
  • Meningitis
  • Leprosy
127
Q

Bacteria can grow elsewhere and release toxins that affect neurons… examples include:

A
  • Botulism
  • Tetanus
128
Q

Viruses more readily cross the blood-brain barrier… examples include:

A
  • Meningitis
  • Polio
  • Rabies
  • Encephalitis
129
Q

Fungal infections of the nervous system spread from the ______ to the CNS via the blood.

130
Q

Fungal toxins can produce (in the CNS):

A
  • Hallucinations
  • Neurological problems
  • Fungal meningitis
131
Q

Protozoan infections of the nervous system are rare and include…?

A
  • Trypanosomiasis (African sleeping sickness)
  • Amebic meningoencephalitis
132
Q

Prions cause what in the brain?

A

Spongiform encephalopathies

133
Q

What are the signs and symptoms of bacterial meningitis?

A
  • Sudden high fever & severe meningeal inflammation
  • Increased WBCs in the cerebrospinal fluid (CSF)
  • Infection of the brain causes encephalitis resulting in behavioural changes, coma, and death
134
Q

5 species cause __% of bacterial meningitis cases.

135
Q

What are the 5 species that cause bacterial meningitis cases?

A
  1. Neisseria meningitidis
  2. Streptococcus pneumoniae
  3. Haemophilus influenzae
  4. Listeria monocytogenes
  5. Streptococcus agalactiae
  6. Opportunistic members of the normal microbiome can also cause meningitis
136
Q

Neisseria meningitidis is also known as…?

A

Meningococcus

137
Q

Describe Neisseria meningitidis and its virulence factors in causing meningitis.

A
  • Gram-negative cocci
  • Fimbria help the bacteria attach to cells (Neisseria cells without these structures are avirulent)
  • Capsule protects bacteria from phagocytic lysis
  • Release of Lipid A from LPS into the body triggers fever, inflammation, shock, and blood clotting
138
Q

Streptococcus pneumoniae is also known as…?

A

Pneumococcus

139
Q

Leading cause of meningitis in children and eldery.

A

Streptococcus pneumoniae

140
Q

Describe Streptococcus pneumoniae and its virulence factors in causing meningitis.

A
  • Gram-positive coccus
  • Capsule protects bacteria from digestion by phagocytes
  • Enzymes and toxins enable bacteria to counteract immune defenses
  • Phosphorylcholine in bacterial cell wall triggers endocytosis by cells
141
Q

Describe Haemophilus influenzae and its virulence factors in causing meningitis.

A
  • Pleomorphic bacillus
  • Obligate parasite of humans and some animals
  • Presence of capsule resists phagocytosis
  • Different Haemophilus strains distinguished by capsular antigens (6 different strains)
  • Prior to introduction of an effective vaccination, most disease caused by H. influenzae type B
142
Q

How many different strains of Haemophilus are there? How are they distinguished?

A
  • 6 different strains
  • Distinguished by capsular antigens
143
Q

Describe Listeria monocytogenes and its virulence factors in causing meningitis.

A
  • Gram-positive coccobacillus
  • Enters the body in contaminated food or drink
  • Rarely pathogenic in healthy adults
  • Meningitis can occur in pregnant women, fetuses, newborns, and the elderly or immunocompromised
  • Production of listeriolysin O protects the bacteria from phagocytic digestion
144
Q

Production of what protects Listeria monocytogenes from phagocytic digestion?

A

Listeriolysin O

145
Q

Describe the pathogenesis of listeriosis and how it can lead to meningitis.

A
  1. Listeria enters the body usually through contaminated food/drink
  2. Listeria triggers its own phagocytosis by a host cell, typically in the gallbladder
  3. The intracellular bacterium escapes the phagosome & reproduces within the phagocyte
  4. The bacterium polymerizes the host cell’s actin filaments into a “tail”
  5. The tail pushes the bacterium into a pseudopod
  6. The pseudopod is endocytized by a new host cell
  7. The cycle repeats as the bacterium reproduces within the new host cell
  8. After spending some time within cells, Listeria can travel via the blood to the brain, where it causes meningitis
146
Q

Why does Listeria reproduce more rapidly inside human cells?

A

Some of the mRNA in a Listeria cell activate at 37C.

147
Q

Describe Streptococcus agalactiae and its virulence factors in causing meningitis.

A
  • Lancefield group B streptococcus
  • Normal vaginal microbiota in some women
  • Causes bacteremia, pneumonia, and meningitis in newborns
  • Capsule allows bacteria to evade phagocytosis
148
Q

______ or ______ trauma may allow entry of bacteria into meninges.

A

Head or neck trauma.

149
Q

Was leading cause of bacterial meningitis prior to vaccination.

A

Haemophilus influenzae

150
Q

Leading cause of bacterial meningitis in newborns.

A

Streptococcus agalactiae

151
Q

Meningococcal meningitis can become epidemic among individuals where?

A

Spreads among individuals in barracks and dorms.

152
Q

Is not transmitted among humans except from mother to fetus.

153
Q

Vaccines are available for what species that cause bacterial meningitis?

A
  • S. pneumoniae
  • H. influenzae type b
  • N. meningitidis
154
Q

Administration of ________ at birth reduces neonatal meningitis due to S. agalactiae.

A

Penicillin

155
Q

Describe the signs and symptoms of Hansen’s disease (leprosy).

A
  • Tuberculoid leprosy = non-progressive form of the disease (loss of sensation in skin lesions, strong cell-mediated immune response)
  • Lepromatous leprosy = progressive tissue destruction (due to bacterial replication in the skin, mucous membranes, and nerves cells; weak cell-mediated immune response)
  • Death from leprosy is rare
156
Q

What is the non-progressive vs. progressive form of leprosy called?

A
  • Non-progressive = Tuberculoid leprosy
  • Progressive = Lepromatous leprosy
157
Q

Describe the pathogen that causes leprosy.

A
  • Caused by Mycobacterium leprae
  • Gram-positive bacillus (AFB = acid-fast bacillus)
  • Mycolic acid in the cell wall is responsible for several characteristics of the bacterium (slow growth rate, protection from phagocytic lysis, growth within phagocytes, resistance to many antimicrobial drugs)
158
Q

Describe the pathogenesis of leprosy.

A
  • M. leprae grows best in cooler regions of the body (peripheral nerve endings, mucous membrane, and skin cells)
  • M. leprae can live inside infected cells for years
  • Cellular immune response eventually attacks infected cells; may destroy nerves and other tissues
159
Q

Describe the epidemiology of leprosy.

A
  • Lepromatous leprosy is becoming rare
  • Transmitted by person-to-person contact or breaks in the skin
  • Leprosy is NOT highly virulent (infection after prolonged exposure
160
Q

What vaccine may provide some protection against leprosy?

A

BCG (tuberculosis) vaccine

161
Q

Botulism is an intoxication with 3 manifestations… what are those?

A
  1. Foodborne botulism (botulism toxin in contaminated food)
  2. Infant botulism (results from ingestion of the bacterium C. botulinum; grows in the child’s GI tract and produces toxin)
  3. Wound botulism (contamination of a wound by endospores)
162
Q

What are the signs and symptoms associated with the 3 manifestations of botulism?

A
  • Foodborne: progressive paralysis on both sides of the body; blurred vision, dry mouth, nausea, abdominal pain; slow recovery from growth of new nerve cell endings; death may occur from paralysis of diaphragm
  • Infant: non-specific symptoms (constipation, failure to thrive)
  • Wound: similar symptoms as foodborne (longer incubation period; 4 days or more)
163
Q

Describe the pathogen that causes botulism.

A
  • Caused by Clostridium botulinum
  • Anaerobic, Gram-positive, endospore-forming bacillus (survives improper canning of non-acidic food)
  • Common worldwide in soil and water
  • Different strains produce 1 of 7 neurotoxins (considered the deadliest toxin known; used in botox treatment); act at neuromuscular junctions
164
Q

Considered the deadliest toxin known.

A

Neurotoxins (produced by Clostidrium botulinum)

165
Q

What manifestation of botulism is more common in the USA?

A

Infant botulism

166
Q

What are the 4 approaches to treatment for botulism?

A
  1. Maintain open and functional airways
  2. Wash intestinal tract to remove Clostridium
  3. Administer botulism immunoglobulin
  4. Treat with antimicrobial drugs (wound botulism)
167
Q

How can botulism be prevented?

A
  • By destroying endospores in contaminated food
  • Infants < 1y/o should not consume honey
168
Q

What are the signs and symptoms of tetanus?

A
  • Tightening of the jaw and neck muscles (lockjaw)
  • Spasms and contractions may spread to other muscles
  • Irregular heartbeat/BP and profuse sweating may occur
169
Q

Describe the pathogen that causes tetanus.

A
  • Caused by Clostridium tetani
  • Anaerobic, Gram-positive, endospore-forming bacillus
  • Endospores survive in soil, dust, and the intestines of humans and animals
  • Produce neurotoxin called tetanospasmin (released when bacterial cells die)
170
Q

What is the toxin produced by Clostridium tetani that causes tetanus called?

A

Tetanospasmin

171
Q

Describe the action of tetanus toxin (tetanospasmin) on a pair of antagonistic muscles.

A
  • Tetanospasmin blocks release of inhibitory neurotransmitter
  • = Muscles fully contracted (cannot relax)
172
Q

How can you acquire Clostridium tetani (i.e. tetanus)?

A

Through break in skin or mucous membrane.

173
Q

Distance of infection from CNS determines incubation period of what disease?

174
Q

Describe the epidemiology of tetanus.

A
  • Mortality rate is ~50% if left untreated
  • Incidence has decreased worldwide
  • Most cases occur where immunization or adequate medical care is unavailable
175
Q

Treatment of tetanus involves what steps?

A
  • Thorough wound cleaning
  • Passive immunotherapy
  • Administration of antimicrobials
  • Active immunization
176
Q

What vaccine is used against tetanus? What type of vaccine is this?

A

DTaP vaccine = toxoid (inactivated toxin) vaccine

177
Q

What are the signs and symptoms of viral meningitis?

A
  • Usually milder than bacterial/fungal
  • Fever, headache, stiff-neck, drowsiness, confusion
  • Meningeal inflammation causes most of the symptoms
178
Q

Describe the pathogens that cause viral meningitis?

A
  • About 90% of cases caused by genus Enterovirus (small +ssRNA viruses): Coxsackie A/B virus, echovirus
  • Herpesviruses and mumps virus may cause some cases
  • Spread via fecal contamination of food, water, or hands
  • Spread by the bloodstream (viremia) to other organs following ingestion
179
Q

About 90% of viral meningitis cases are caused by viruses in what genus? What are some examples of those viruses?

A
  • Enterovirus
  • Examples: Coxsackie A/B virus, echovirus
180
Q

Describe the pathogenesis of viral meningitis.

A
  • Incubation period is 3-7 days
  • The virus spreads from the intestine and lungs via the bloodstream
  • Virus is cytolytic; damage to cells in the meninges triggers meningitis
181
Q

Describe the epidemiology of viral meningitis.

A
  • More common than bacterial and fungal meningitis
  • Spread via respiratory droplets and feces
182
Q

Patients recover from viral meningitis without treatment after _____ days.

183
Q

What are the signs and symptoms of poliomyelitis (polio)?

A
  • Asymptomatic infections are almost 90% of cases
  • Minor polio: non-specific symptoms (fever, headache, malaise, sore throat)
  • Non-paralytic polio: muscle spasms, back pain (+ symptoms from minor)
  • Paralytic polio: paralysis by limiting nerve impulse conduction (infection of the spinal cord and cerebrum)
  • Postpolio syndrome: deterioration of polio-affected muscle functions in up to 80% of recovered polio patients (some 30-40 years after the primary infection)
184
Q

Describe the pathogen that causes poliomyelitis.

A
  • Caused by Poliovirus
  • Transmitted most often by drinking contaminated water
  • Poliovirus replicates in the cells of the throat and intestines before spreading via lymph/blood to infect neurons in the CNS
185
Q

Describe the epidemiology of poliomyelitis.

A
  • Epidemics of polio were common in the past
  • Fewer than 50 naturally acquired cases in 2018
  • Polio only exists endemically in regions in South Asia
186
Q

What are the 2 vaccines available against poliomyelitis?

A
  1. Salk vaccine (inactivated polio vaccine = IPV)
  2. Sabin vaccine (attenuated, oral polio vaccine = OPV)
187
Q

Describe the advantages of the Salk vaccine.

A
  • Effective
  • Inexpensive
  • Stable during transport and storage
  • Poses NO risk of vaccine-related disease
188
Q

Describe the disadvantages of the Salk vaccine.

A
  • Requires booster to achieve life-long immunity
  • Must be injected
  • Requires higher community immunization rate than does OPV
189
Q

Describe the advantages of the Sabin vaccine.

A
  • Provides life-long immunity without boosters
  • Triggers secretory antibody response similar to natural infection
  • Easy to administer
  • Results in herd immunity
190
Q

Describe the disadvantages of the Sabin vaccine.

A
  • Less stable than IPV
  • Can mutate to disease-causing form
  • Poses risk of development of polio in immunocompromised contacts of immunized individuals
191
Q

What are the signs and symptoms of rabies?

A
  • Initial symptoms include pain, itching at site of infection, fever, headache, malaise, anorexia
  • Characteristic neurological signs if virus reaches CNS: hyperaggression, hydrophobia, seizures, disorientation, hallucination, and paralysis
192
Q

Describe the pathogen that causes rabies.

A
  • Caused by Rabies virus (-ssRNA virus)
  • Helical capsid supercoiled into cylinded
  • Bullet-shaped envelope
193
Q

Describe the pathogenesis of rabies.

A
  • Transmitted via bite or scratch from an infected animal
  • Virus replicates in muscle cells
  • Virus then moves across neuromuscular junctions into neurons and travels to the CNS via axonal transport
194
Q

Describe the epidemiology of rabies.

A
  • Zoonotic disease (affects mammals)
  • Bats are the source of most cases of rabies in humans
  • Skunks, foxes, or raccoons are the predominant wildlife reservoirs for rabies in some portions of the USA
195
Q

What is the source of most cases of rabies in humans?

196
Q

How is rabies diagnosed?

A
  • Diagnosis by unique neurological symptoms and test for antibodies
  • Postmortem detection of Negri bodies (viral aggregates) in the brain
197
Q

What are Arboviruses?

A
  • Arboviruses are arthropod-borne viruses (transmitted via blood-sucking arthropods like mosquitoes)
  • Zoonotic diseases (infect different species); rarely affect humans
198
Q

What are the signs and symptoms of Arboviral encephalitis?

A
  • Arboviruses usually cause mild, cold-like symptoms
  • Can cause encephalitis if crosses the blood-brain barrier; symptoms similar to meningitis
199
Q

Describe the types of arboviruses that cause Arboviral encephalitis.

A
  • 6 arboviruses belonging to 3 families cause most cases in NA
    1. Togaviridae: Eastern equine encephalitis (EEE), Western
      equine encephalitis (WEE), and Venezuelan equine encephalitis
      (VEE) virus
      1. Flaviviridae: St. Louis encephalitis and West Nile virus (WNV = most significant cause in NA)
      2. Bunyaviridae: California LaCrosse Encephalitis virus
200
Q

What type of arbovirus is the most significant cause of Arboviral encephalitis in NA?

A

West Nile virus

201
Q

Describe the pathogenesis of Arboviral encephalitis.

A
  • Transmission to humans by female Aedes/Culex mosquitoes
  • Arboviruses enter cells via endocytosis and replicate in them
  • Arboviruses produce viremia (triggers swollen lymph nodes) and cross the blood-brain barrier
202
Q

Why can’t horses and humans infect mosquitoes with arboviruses?

A

Viremia is not high enough in humans/horses to infect mosquitoes.

203
Q

Describe the epidemiology of Arboviral encephalitis.

A
  • Birds and rodents are the normal hosts
  • People who engage in outdoor activities in endemic
    areas are at risk for infection (older adults and children are
    at higher risk)
  • Incidence of arboviral encephalitis is seasonal (when mosquito #s are high)
204
Q

Vaccine (for horses) are available for what types of arboviruses?

A
  • EEE
  • WEE
  • VEE
  • WNV
205
Q

What are the signs and symptoms of Zika virus disease?

A
  • Often asymptomatic
  • Infections in pregnant women can cause congenital Zika syndrome: infants may be born with brain abnormalities and microcephaly (may also disrupt normal development of the heart, digestive system, or genitalia)
206
Q

Describe the pathogenesis of Zika virus disease.

A
  • Transmitted via mosquito bite or sexual activity
  • Zika virus preferentially replicates in brain cells
207
Q

Describe the epidemiology of Zika virus disease.

A
  • Zika virus discovered in Africa in the 1940s
  • Cases have spread to the Americas and the Caribbean
208
Q

What are the signs and symptoms of cryptococcal meningitis?

A
  • Similar to those of bacterial meningitis
  • Loss of vision and coma may occur in later stages
209
Q

Describe the pathogen that causes cryptococcal meningitis.

A
  • Caused by fungus Cryptococcus neoformans
  • Found in soil and some bird feces
  • Polysaccharide capsule provides resistance to phagocytosis
210
Q

Describe the pathogenesis of cryptococcal meningitis.

A
  • Infection follows inhalation of spores or dried yeast cells
  • Spreads via the blood and infects both meninges and brain tissue
  • Many cases occur in terminal AIDS patients
211
Q

What are the 3 clinical stages of trypanosomiasis (African sleeping sickness)?

A
  1. Site of bite (by Tsetse fly) becomes lesion
  2. Parasites in the blood create fever, lymph node swelling, and headache
  3. Protozoa invades CNS, causing meningoencephalitis
212
Q

What is trypanosomiasis characterized by?

A

Cyclic waves of parasitemia.

213
Q

Describe the pathogen that causes trypanosomiasis.

A
  • Caused by protozoa Trypanosoma brucei
  • Evades immune system by changing surface glycoproteins
214
Q

Describe the epidemiology of trypanosomiasis.

A

Occurs in equatorial and subequatorial savanna and riverine areas of Africa, wherever Tsetse flies live.

215
Q

What are the signs and symptoms of primary amebic meningoencephalopathy?

A
  • Fever, headache, stiff neck, altered mental state
  • Progressively worsens until the patient dies
216
Q

Describe the pathogens that cause primary amebic meningoencephalopathy.

A
  • Caused by 2 amoebas: Acanthamoeba & Naegleria
  • Free-living inhabitants of water bodies, moist soil, AC units, humidifiers, etc.
  • Enter host through abrasions on the skin/eyelid, or by inhalation of contaminated water
  • Rare but almost always fatal
217
Q

What is a prion? What can it cause?

A
  • A prion is an infectious protein
  • Cause spongiform encephalopathies (brains of victims full of holes): VCJD in humans, scrapie in sheep, and “mad cow” disease in cattle
218
Q

What are the signs and symptoms of Variant Creutzfeldt-Jakob Disease (VCJD)?

A
  • Insomnia, weight loss, and memory failure
  • Progressive worsening of muscle control
  • Death usually occurs within 12 months
219
Q

Describe the pathogenesis of VCJD.

A
  • Caused by abnormal form of prion that turns normal prions into abnormal form
  • Can spread via medical procedures
  • Prions may remain dormant for many years
  • VCJD can occur in young people
220
Q

Leading cause of non-traumatic blindness.

221
Q

What are the signs and symptoms of trachoma?

A
  • Scarring of the conjunctiva and cornea
  • Purulent discharge and deformed eyelids
222
Q

Describe the pathogen that causes trachoma.

A
  • Caused by Chlamydia trachomatis
  • Bacterium multiples in the conjunctiva
  • Scarring triggers invasion by blood vessels and eventually leads to blindness
  • Typically affects children infected during birth
223
Q

Bacterial infections of the ______ and ______________ can affect the eyes.

A
  • Skin
  • Reproductive tract
224
Q

Infections of the sebaceous glands near the eye are called…? They are caused by what pathogen…?

A
  • Sties
  • Caused by Staphylococcus aureus
225
Q

What is Opthalamia neonatorum? What pathogen is it caused by?

A
  • Inflammation of the conjunctiva and cornea of a newborn
  • Caused by Neisseria gonorrhoeae
226
Q

What is a common bacterial cause of conjunctivitis (inflammation of the conjunctiva)?

A

Haemophilus influenzae

227
Q

FIRST PART OF LECTURE 15

Medical Microbiology (3 decks)

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