INFECTIONS IN THE IMMUNOCOMPROMISED HOST
Infections can be caused by either common bacteria or unusual bacteria, viruses, protozoa,
helminthes, or fungi. Patients underlying immune status needs to be considered. Neutropenia
is frequently associated with mucosal disruption, and the indigenous colonizing florae are
responsible for most infections. Pathogens causing initial infections are usually bacterial,
including both gram-positive and gram-negative organisms. Pathogens causing subsequent
infections are usually antibiotic-resistant bacteria, yeast, or fungi. Acute disseminated
candidiasis in neutropenic host can have an erythematous or hemorrhagic palpable rash,
which is consistent with small vessel vasculitis (75).Fusarium sp. can begin as multiple
erythematous macules, papules, and necrotic nodules. Primary cutaneous zygomycosis is seen
with disruption of skin in immunocompromised patients and patients with burns or severe
soft tissue trauma. It starts as erythema and induration of the skin at a puncture site and
progresses to necrosis. In neutropenic patient’s local necrosis, tissue infarction, vessel invasion,
and dissemination can occur (76,77).
Patients with cellular immune deficiency are at increased risk of infection with
Mycobacterium, which can manifest as cellulitis, painless nodules, necrotic ulcers, and
abscesses. Bacillary angiomatosis (epitheliod angiomatosis), primarily involves the skin and
visceral organs in patient with AIDS, is due toBartonella henselaeor Bartonellaquintana. Lesions
can occur as red papules or painful cutaneous nodules. Histologically, consist of circum-
scribed, lobular proliferation of capillaries lined with prominent large endothelial cells.
CutaneousNocardiainfection usually represents metastatic infection. CutaneousCryptococcus
infection can appear as papules, nodules, pustules, or necrotic ulcers. Cutaneous manifestation
of acute disseminated histoplasmosis are rare, and they appear as nonspecific maculopapular
eruptions that may become hemorrhagic. Varicella zoster virus can cause dissemination
complicated by secondary bacterial and fungal super infection. Herpes simplex virus lesions
frequently coalesce and ulcerate. Skin and soft tissue infection can rarely be infected by
parasites (Strongyloides stercoralis,Sarcoptes scabiei,Acanthamoebasp., andBalamuthia).
Biopsy and culture of suspicious lesions frequently are necessary to diagnose these
pathogens.
Ecthyma Gangrenosum
Ecthyma gangrenosum is the classic skin lesion associated withP. aeruginosainfection in
granulocytopenic patients (78–80) and has been reported in 2% to 28% of patients with
Pseudomonasbacteremia. Rarely this lesion may be caused by other organisms including
S. aureus, Aeromonas, Serratia, Klebsiella, E. coli, Capnocytophaga, Aspergillus, and Candida.
Neutropenic patients with overwhelming septicemia develop a patchy dermal and subcuta-
neous necrosis. The characteristic skin lesion starts with erythematous macular eruptions that
become bullous with central ulceration and necrosis. These are usually multiple occurring in
different stages of development, which may concentrate on the extremities or the head and
neck. Ecthyma gangrenosum is a cutaneous vasculitis caused by bacterial invasion of the
media and adventitia of the vessel wall. Diagnosis of the etiological agent may occur with
biopsy of the lesion being cultured or isolated from blood cultures. Treatment is primarily by
administration of IV antimicrobial therapy and by debridement of multiple lesions, which may
lessen the bacterial burden.
SURGICAL SITE INFECTIONS
Incisional surgical site infections (SSIs) can be defined according to national nosocomial
infection surveillance (NNIS) criteria (81). Superficial SSI involves only skin or subcutaneous
tissue of the incision, and in addition SSI includes at least one of the following: (i)purulent
drainage; (ii) isolation of an organism from the site; (iii) at least one of the following clinical
findings: tenderness, redness, or heat along with incision and drainage by the surgeon; or
(iv) diagnosis made by the surgeon or attending physician. Superficial SSI occurs within
30 days following surgery. Deep SSI is defined asinfection involving fascial or muscle layers
of the incision and accompanied by purulent drainage, spontaneous dehiscence, or
intentional opening by a surgeon in a patient with fever, local pain, tenderness, abscess, or
diagnosis by a physician. Deep SSI occurs within 30 days of surgery if no implant is left in
310 Sharma and Saravolatz