52 BACTEriAL vAGiNOSiS
Image 13.1
Clue cells are squamous epithelial cells covered with bacteria found in bacterial vaginosis.
Copyright Noni macDonald, mD. Image 13.2
This photomicrograph reveals bacteria adhering to vaginal epithelial cells known as clue cells.
Clue cells are epithelial cells that have had bacteria adhere to their surface, obscuring their borders, and imparting a stippled appearance.
The presence of such clue cells is a sign the patient has bacterial vaginosis. Courtesy of Centers for Disease Control and Prevention/
m. rein.
bacteria, such as Diagnosit BVBlue (Gryphus Diagnostics, Knoxville, TN) and OSOM BVBlue Test (Sekisui Diagnostics, Lexington, MA), have strong clinical performance com- pared with the Nugent criteria. The FemExam G vaginalis PIP Activity TestCard (Litmus Concepts Inc, Santa Clara, CA) detects proline iminopeptidase activity of anaerobes and can be performed as a point-of-care test in less than 2 minutes.
Sexually active females with BV should be eval- uated for coinfection with syphilis, gonorrhea, chlamydia, trichomoniasis, and HIV. Comple- tion of the hepatitis B and human papillomavi- rus immunization series should be confirmed.
Treatment
Symptomatic patients should be treated.
The goals of treatment are to relieve the symp- toms and signs of infection and to potentially
decrease the risk of infectious complications.
Treatment considerations should include patient preference for oral versus intravaginal treatment, possible adverse effects, and pres- ence of coinfections. Nonpregnant patients may be treated orally with metronidazole or topically with metronidazole gel or clinda- mycin cream. Alternative regimens include oral tinidazole, oral clindamycin, or clinda- mycin intravaginally.
Approximately 30% of appropriately treated females have a recurrence within 3 months.
Retreatment with the same regimen or an alternative regimen are both reasonable options.
Pregnant or breastfeeding women with symp- toms of BV should be treated with oral metro- nidazole or clindamycin. Oral therapies are preferred in pregnancy to treat possible upper genital tract infection.
Image 13.3
Gardnerella vaginalis on chocolate agar. Colonies are small, circular, gray, and convex. Courtesy of Julia rosebush, DO; robert Jerris, PhD; and Theresa Stanley, m(ASCP).
BACTEROIDES AND PREVOTELLA iNFECTiONS 53
14
Bacteroides and Prevotella Infections
Clinical Manifestations
Bacteroides and Prevotella organisms from the oral cavity can cause chronic sinusitis, chronic otitis media, dental infection, peritonsillar abscess, cervical adenitis, retropharyngeal space infection, aspiration pneumonia, lung abscess, pleural empyema, or necrotizing pneumonia. Species from the gastrointestinal tract are recovered in patients with peritonitis, intra-abdominal abscess, pelvic inflammatory disease, postoperative wound infection, or vul- vovaginal and perianal infections. Invasion of the bloodstream from the oral cavity or intesti- nal tract can lead to brain abscess, meningitis, endocarditis, arthritis, or osteomyelitis. Skin and soft tissue infections include synergistic bacterial gangrene and necrotizing fasciitis;
omphalitis in newborns; cellulitis at the site of fetal monitors, human bite wounds, or burns;
infections adjacent to the mouth or rectum;
and infected decubitus ulcers. Neonatal infec- tions, including conjunctivitis, pneumonia, bacteremia, or meningitis, are rare. In most settings where Bacteroides and Prevotella are implicated, the infections are polymicrobial.
Etiology
Most Bacteroides and Prevotella organisms associated with human disease are pleomor- phic, nonspore-forming, facultatively anaero- bic, gram-negative bacilli.
Epidemiology
Bacteroides and Prevotella species are part of the normal flora of the mouth, gastrointestinal tract, and female genital tract. Members of the Bacteroides fragilis group predominate in the gastrointestinal tract flora; members of the Pre
votella melaninogenica (formerly Bacteroides melaninogenicus) and Prevotella oralis (for- merly Bacteroides oralis) groups are more com- mon in the oral cavity. These species cause infection as opportunists, usually after an alteration in skin or mucosal membranes in conjunction with other endogenous species.
Endogenous infection results from aspiration, bowel perforation, or damage to mucosal sur- faces from trauma, surgery, or chemotherapy.
Mucosal injury or granulocytopenia predis- pose to infection. Enterotoxigenic B fragilis may be a cause of diarrhea. Except in infections resulting from human bites, no evidence of person-to-person transmission exists.
Incubation Period
Usually 1 to 5 days (depending on inoculum and body site).
Diagnostic Tests
Anaerobic culture media are necessary for recovery of Bacteroides or Prevotella species.
Because infections usually are polymicrobial, aerobic cultures should also be obtained. A putrid odor suggests anaerobic infection. Use of an anaerobic transport tube or a sealed syringe is recommended for collection of clini- cal specimens.
Treatment
Abscesses should be drained when feasible;
abscesses involving the brain, liver, and lungs may resolve with effective antimicrobial ther- apy. Necrotizing soft tissue lesions should be debrided surgically and can require repeated surgeries.
The choice of antimicrobial agent(s) is based on anticipated or known in vitro susceptibility testing. Bacteroides infections of the mouth and respiratory tract generally are susceptible to penicillin G, ampicillin, and extended- spectrum penicillins, such as ticarcillin or piperacillin. Clindamycin is active against virtually all mouth and respiratory tract Bacteroides and Prevotella isolates and is recommended by some experts as the drug of choice for anaerobic infections of the oral cavity and lungs but is not recommended for central nervous system infections. Some spe- cies of Bacteroides and almost 50% of Prevotella species produce β-lactamase. A β-lactam penicillin active against Bacteroides species combined with a β-lactamase inhibitor ( ampicillin-sulbactam, amoxicillin-clavulanate, ticarcillin-clavulanate, or piperacillin- tazobactam) can be useful to treat these infec-
54 BACTEROIDES AND PREVOTELLA iNFECTiONS
tions. Bacteroides species of the gastrointestinal tract usually are resistant to penicillin G but are predictably susceptible to metronidazole, β-lactam plus β-lactamase inhibitors, chloram-
phenicol, and, sometimes, clindamycin. More than 80% of isolates are susceptible to cefoxitin and meropenem. Cefuroxime, cefotaxime, and ceftriaxone are not reliably effective.
Image 14.1
Bacteroides fragilis pneumonia in a newborn (B fragilis isolated from the placenta and blood culture from the newborn). Anaerobic cultures were obtained because of a fecal odor in the amniotic fluid.
Image 14.2
Prevotella melaninogenica (previously Bacteroides melaninogenicus) and group A α-hemolytic strep- tococcus cultured from a submandibular subcu- taneous abscess aspirate from a 12-year-old boy.
There was no apparent dental, pharyngeal, or middle ear infection.
Image 14.3
Bacteroides fragilis abdominal abscess in a 9-year-old boy. Courtesy of Benjamin Estrada, mD.
Image 14.4
This photomicrograph shows Bacteroides fragilis after being cultured in a thioglycollate medium for 48 hours. B fragilis is a gram-negative rod that constitutes 1% to 2% of the normal colonic bacterial microflora in humans. it is associated with extraintestinal infections such as abscesses and soft tissue infections, as well as diarrheal diseases. Courtesy of Centers for Disease Control and Prevention/Dr v. r. Dowell Jr.
BACTEROIDES AND PREVOTELLA iNFECTiONS 55
Image 14.5
Prevotella melaninogenica pigmented colonies. Courtesy of Centers for Disease Control and Prevention.
Image 14.6
Bacteroides fragilis on kanamycin-vancomycin–laked blood agar. The organism is not inhibited by kanamycin and vancomycin and, thus, demonstrates good growth on this agar. Courtesy of Julia rosebush, DO; robert Jerris, PhD; and Theresa Stanley, m(ASCP).
56 BALANTIDIUM COLI iNFECTiONS
15
Balantidium coli Infections
(Balantidiasis)
Clinical Manifestations
Most human infections are asymptomatic.
Acute symptomatic infection is characterized by rapid onset of nausea, vomiting, abdominal discomfort or pain, and bloody or watery mucoid diarrhea. In some patients, the course is chronic with intermittent episodes of diar- rhea, anorexia, and weight loss. Rarely, organ- isms spread to mesenteric nodes, pleura, lung, liver, or genitourinary sites. Inflammation of the gastrointestinal tract and local lymphatic vessels can result in bowel dilation, ulceration, perforation, and secondary bacterial invasion.
Colitis produced by Balantidium coli often is indistinguishable from colitis produced by Entamoeba histolytica. Fulminant disease can occur in patients who are malnourished or otherwise debilitated or immunocompromised.
Etiology
B coli, a ciliated protozoan, is the largest patho- genic protozoan known to infect humans.
Epidemiology
Pigs are the primary host reservoir of B coli, but other sources of infection have been reported. Infections have been reported in
most areas of the world but are rare in indus- trialized countries. Cysts excreted in feces can be transmitted directly from hand to mouth or indirectly through fecally contaminated water or food. Excysted trophozoites infect the colon. A person is infectious as long as cysts are excreted in stool. Cysts may remain viable in the environment for months.
Incubation Period
Unknown but may be several days.
Diagnostic Tests
Diagnosis of infection is established by scraping lesions via sigmoidoscopy, histologic examination of intestinal biopsy specimens, or ova and parasite examination of stool. Diag- nosis is usually established by demonstrating trophozoites (or, less frequently, cysts) in stool or tissue specimens. Stool examination is less sensitive, and repeated stool examination is necessary to diagnose infection because shed- ding of organisms can be intermittent. Micro- scopic examination of fresh diarrheal stools must be performed promptly because tropho- zoites degenerate rapidly.
Treatment
The drug of choice is a tetracycline. Alterna- tive drugs are metronidazole and iodoquinol.
Successful use of nitazoxanide has also been reported.
Image 15.1
Balantidium coli trophozoites are characterized by their large size (40–>70 µm); the presence of cilia on the cell surface, which are particularly visible (B); a cytostome (arrows); a bean-shaped macronucleus that is often visible (A); and a smaller, less conspicuous micronucleus.
Courtesy of Centers for Disease Control and Prevention.
Image 15.2
Balantidium coli cyst in stool preparation.
Courtesy of Centers for Disease Control and Prevention/Dr L.L.A. moore Jr.
BALANTIDIUM COLI iNFECTiONS 57
Image 15.3
Cysts are the parasite stage responsible for transmission of balantidiasis (1). The host most often acquires the cyst through ingestion of contaminated food or water (2). Following ingestion, excystation occurs in the small intestine, and the trophozoites colonize the large intestine (3). The trophozoites reside in the lumen of the large intestine of humans and animals, where they replicate by binary fission, during which conjugation may occur (4). Trophozoites undergo encystation to produce infective cysts (5). Some trophozoites invade the wall of the colon and multiply. Some return to the lumen and disintegrate. mature cysts are passed with feces (1). Courtesy of Centers for Disease Control and Prevention/Alexander J. da Silva, PhD/melanie moser.
58 BAYLISASCARIS iNFECTiONS
16
Baylisascaris Infections
Clinical Manifestations
Baylisascaris procyonis, a raccoon roundworm, is a rare cause of acute eosinophilic meningo- encephalitis. In a young child, acute central nervous system (CNS) disease (eg, altered men- tal status, seizures) accompanied by peripheral or cerebrospinal fluid (CSF) eosinophilia occurs 2 to 4 weeks after infection. Severe neu- rologic sequelae or death are usual outcomes.
B procyonis is also a rare cause of extraneural disease in older children and adults. Ocular larva migrans can result in diffuse unilateral subacute neuroretinitis; direct visualization of worms in the retina is sometimes possible.
Visceral larval migrans can present with non- specific signs, such as macular rash, pneumo- nitis, and hepatomegaly. Similar to visceral larva migrans caused by Toxocara, subclinical or asymptomatic infection is thought to be the most common outcome of infection.
Etiology
B procyonis is a 10- to 25-cm long roundworm (nematode) with a direct life cycle usually limited to its definitive host, the raccoon.
Domestic dogs and some exotic pets, such as kinkajous and ringtails, can serve as definitive hosts and a potential source of human disease.
Epidemiology
B procyonis is distributed focally throughout the United States; in areas where disease is endemic, an estimated 22% to 80% of raccoons can harbor the parasite in their intestine.
Reports of infections in dogs raise concern that infected dogs may be able to spread the disease. Embryonated eggs containing infec- tive larvae are ingested from the soil by rac- coons, rodents, and birds. When infective eggs or an infected host is eaten by a raccoon, the larvae grow to maturity in the small intestine, where adult female worms shed millions of eggs per day. Eggs become infective after 2 to 4 weeks in the environment and may persist long-term in the soil. Fewer than 25 cases of Baylisascaris disease have been document in the United States, although cases may be undi- agnosed or underreported.
Risk factors for Baylisascaris infection include contact with raccoon latrines (bases of trees, unsealed attics, or flat surfaces such as logs, tree stumps, rocks, decks, and rooftops) and uncovered sandboxes, geophagia/pica, age younger than 4 years, and, in older children, developmental delay. Nearly all reported cases have been in males.
Incubation Period Unknown.
Diagnostic Tests
Baylisascaris infection is confirmed by identifi- cation of larvae in biopsy specimens. Serologic testing (serum, CSF) is available at the Centers for Disease Control and Prevention. A pre- sumptive diagnosis can be made on the basis of clinical (meningoencephalitis, diffuse uni- lateral subacute neuroretinitis, pseudotumor), epidemiologic (raccoon exposure), and labora- tory (blood and CSF eosinophilia) findings.
Neuroimaging results can be normal initially, but as larvae grow and migrate through CNS tissue, focal abnormalities are found in peri- ventricular white matter and elsewhere. In ocular disease, ophthalmologic examination can reveal characteristic chorioretinal lesions or, rarely, larvae. Because eggs are not shed in human feces, stool examination is not helpful.
Treatment
On the basis of CNS and CSF penetration and in vitro activity, albendazole, in conjunction with high-dose corticosteroids, has been advo- cated most widely but may not affect clinical outcome in severe CNS infections. If suspected, treatment should be started while the diagnos- tic evaluation is being completed. Some experts advocate use of additional anthelmintic agents.
Limited data are available on safety and effi- cacy of these therapies in children. Preventive therapy with albendazole should be considered for children with a history of ingestion of soil potentially contaminated with raccoon feces.
Worms localized to the retina may be killed by direct photocoagulation.
BAYLISASCARIS iNFECTiONS 59
Image 16.3
Coronal T2-weighted magnetic resonance imaging of the brain in a 4-year-old with Baylisascaris procyonis eosinophilic meningitis.
Arrow shows diffuse edema of the superior cerebellar hemispheres (scale bar increments in centimeters). Courtesy of Centers for Disease Control and Prevention/Emerging Infectious Diseases and Poulomi J. Pai.
Image 16.4
unembryonated egg of Baylisascaris procyonis.
B procyonis eggs are 80 to 85 µm by 65 to 70 µm in size, thick-shelled, and usually slightly oval in shape. They have a similar morphology to fertile eggs of Ascaris lumbricoides, although eggs of A lumbricoides are smaller (55–75 µm x 35–50 µm).
The definitive host for B procyonis is the raccoon, although dogs may also serve as definitive hosts.
As humans do not serve as definitive hosts for B procyonis, eggs are not considered a diagnos- tic finding and are not excreted in human feces.
Courtesy of Cheryl Davis, mD, Western Kentucky university.
Image 16.1
Neuroimaging of human Baylisascaris procyonis neural larval migrans. Axial T2-weighted magnetic resonance image (at the level of the lateral ventricles) demonstrates abnormal patchy hyperintense signal of periventricular white matter and basal ganglia. Courtesy of Gavin.
Image 16.2
Biopsy-proven Baylisascaris procyonis encephalitis in a 13-month-old boy. Axial T2-weighted magnetic resonance images obtained 12 days after symptom onset show abnormal high signal throughout most of the central white matter (arrows) compared with the dark signal expected at this age (broken arrows).
Sorvillo F, Ash Lr, Berlin OGW, yatabe J, Degiorgio C, morse SA. Baylisascaris procyonis:
an emerging helminthic zoonosis. Emerg Infect Dis. 2002;8(4):355–359.
60 BAYLISASCARIS iNFECTiONS
Image 16.5
Baylisascaris procyonis larva in cross-section (at midbody level) (diameter, 60 µm) recovered from the cerebrum of a rabbit with neural larval migrans. Characteristic features include a centrally located (slightly compressed) intestine, flanked on either side by large triangular-shaped excretory columns.
Prominent lateral cuticular alae are visible on opposite sides of the body (hematoxylin-eosin stain).
Courtesy of Gavin.
Image 16.6
This illustration depicts the life cycle of Baylisascaris procyonis, the causal agent of Baylisascaris disease. Courtesy of Centers for Disease Control and Prevention/Alexander J. da Silva, PhD/
melanie moser.
BAYLISASCARIS iNFECTiONS 61
Image 16.7
Baylisascaris is raccoon roundworm, which may cause ocular and neural larval migrans and encephalitis in humans. Photo used with permission of michigan DNr Wildlife Disease Lab.
62 iNFECTiONS WiTH BLASTOCYSTIS HOMINIS AND OTHEr SuBTyPES
17