Cellulitis Case Tx737

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Human Facial Cowpox Obtained from a Cat • CID 2006:43 (15 September) • 737

R E V I E W A R T I C L E

A Case of Facial Cellulitis and Necrotizing

Lymphadenitis due to Cowpox Virus Infection

Roland Pahlitzsch,1 Anna-Lena Hammarin,2 and Anders Widell3

1Department of Otolaryngology, Blekinge County Hospital, Karlskrona, 2Department of Virology, Swedish Institute of Infectious Disease Control,

Stockholm, and 3Department of Medical Microbiology, Malmo University Hospital, Lund University, Malmo, Sweden

We describe a patient with facial cellulitis/erysipelas due to cowpox virus inoculation in the respiratory

epithelium of the nose. A cytopathic agent was isolated in cell culture, and the diagnosis of cowpox was

confirmed by electron microscopy and polymerase chain reaction. The most likely source of infection was

exposure to the family cats. In addition to the severe edematous cellulitis of the face, the clinical course was

dominated by several areas of subcutaneous, necrotizing lymphadenitis, from one of which a huge abscess

formed that had to be incised. Hyperbaric oxygen treatment was provided to prevent development of dermal

necrosis. The healing process in the numerous areas of lymphadenitis was markedly protracted, and 1 persisting

node (which yielded positive results on polymerase chain reaction) had to be excised 2 years after onset of

disease. This is the first reported case of inoculation of cowpox virus in the respiratory mucosa of the nose.

It resulted in a clinical course totally different than that for inoculation in the skin. We also present a short

review of findings on orthopoxvirus infection that focuses on the chain of transmission.

Facial infection of the skin and soft tissues can be due

to a number of bacterial agents, but it can also be due

to viruses such as herpes simplex virus type 1, varicella

zoster virus, and a range of poxviruses. Formerly, va-

riola virus had humans as its exclusive host, but with

its eradication through mass vaccination, the totalnumber of poxvirus infections has been dramatically

reduced. However, cases of zoonotic poxvirus infection

have occasionally involved humans. Such cases may

present diagnostic difficulties and may have devastating

outcomes [1]. We report a case of cowpox infection

with a prolonged disease course, and we discuss the

viral, diagnostic, epidemiological, and therapeutic

aspects.

CASE REPORT

In early November 2000, a 7-year-old girl living in the

southeast of Sweden sought medical attention from a

Received 28 February 2006; accepted 23 May 2006; electronically published 10

August 2006.

Reprints or correspondence: Dr. Roland Pahlitzsch, Dept. of Otolaryngology,

Blekinge County Hospital, S-37185, Karlskrona, Sweden (roland.pahlitzsch

@ltblekinge.se).

Clinical Infectious Diseases 2006;43:737–42

2006 by the Infectious Diseases Society of America. All rights reserved.

1058-4838/2006/4306-0012$15.00

general practitioner. She presented with an inflamma-

tory, erythematous swelling of the skin beneath the

right ear and painless lymphadenopathy in the regional

parotid and upper jugular lymph nodes. She had no

history of skin injury in the affected region of the head

and neck. Two weeks before the onset of symptoms,the patient had visited Spain. She had received child-

hood vaccinations against mumps, rubella, measles, po-

liomyelitis, Haemophilus influenzae, and diphtheria-tet-

anus-pertussis, but she had not received vaccination

against tuberculosis or smallpox. There was no history

of immunodeficiency or atopia.

The patient had a low-grade fever (temperature,

∼38C) and general malaise, and because a bacterial

infection was suspected, she was treated orally with

penicillin. Despite the administration of treatment, the

symptoms progressed, and the patient was referred to

the Department of Otolaryngology at Blekinge County

Hospital (Karlskrona, Sweden) on 26 November 2000.

Three weeks after the onset of the first symptoms, her

condition worsened. Extensive edema developed in the

upper part of the right side of the neck and on the

right side of the face, extending into the contralateral

side and involving the eyelids; it also developed on the

mental region and the upper part of the right side of

the neck (figure 1A and 1C ).



738 • CID 2006:43 (15 September) • Pahlitzsch et al.

Figure 1. Serial photographs and a CT scan for a patient with facial cowpoxvirus infection. A, Lesion and facial edema 2 weeks after onset of

infection. B, CT obtained 2 weeks after onset. C, Abscess prior to hyperbaric oxygen treatment and surgical incision 6 weeks after onset. D, Status

4 months after hyperbaric oxygen treatment and incision. E, Close-up of long-lasting lesion in medial canthus 24 month after onset. F, Late results,

36 months after onset, showing a minimum of scarring. G, Electron microscopic image of orthopoxvirus obtained from our patient. Consent to appear

in the photographs was obtained from the patient’s guardian.

Physical examination was performed at the time of hospital

admission and revealed a whitish, necrotizing mass in the right

anterior nasal cavity that was surrounded by granulations at

the anterior border of the lower nasal concha. Numerous solid

lymph nodes (diameter, 3–25 mm) were palpable in the right

cheek, near the right nostril, near the right eye (including the

upper eyelid), and more laterally, anterior to the border of the

right parotid gland.

The WBC count ( cells/L) was nearly normal (nor-911.3 10

mal WBC count, ! cells/L). Other laboratory values99.6 10

were slightly elevated: the C-reactive protein level was 14 mg/

mL (normal level, !5 mg/mL), the serum alkaline phosphataselevel was 7.9 mkat/L (normal range, 1.0–4.5 mkat/L), and the

lactate dehydrogenase level was 9.3 mkat/L (normal range, 3.0–

7.0 mkat/L). Plasma electrophoresis revealed a slightly raised

level of IgG3 (1.4 g/L; reference values, 0.13–1.05 g/L), but the

findings were otherwise normal.

Bacteriologic study findings. A nasal swab culture yielded

Streptococcus mitis (low numbers), Haemophilus parainfluenzae

(low numbers), and Neisseria species, including 1 oxidase pos-

itive rod-like bacterium. Samples were obtained for Mycobac-

terium tuberculosis culture, and the results were negative.

The overall interpretation was that the local skin infection

was a phlegmon caused by H. influenzae (although culture re-

sults were negative). Treatment with intravenous cefuroxime

was started on a tentative basis.

Histologic study findings. Biopsy from the nose mass re-

vealed necrotic material with granulocytes.

Radiographic study findings. CT revealed deep edema of

the right cheek, the right parotid gland, and the right side of

the neck. Edema of the respiratory epithelium of the anterior

ethmoidal cells and the nasal concha on the right side couldalso be visualized (figure 1B).

Subsequent clinical course. One week after the acute ex-

acerbation a slight improvement of the cellulitis under the eye

occurred. Around the areas of facial lymphadenitis the skin still

showed a bluish discoloration. However, since the patient’s

general condition improved, she was discharged from the hos-

pital and followed up on weekly visits to our outpatient clinic.

The cellulitis completely resolved within 3 weeks after onset,




but the lymphadenitis in the buccal and periorbital areas de-

veloped into subcutaneous abscess cavities, which ranged in

size from 3 to 40 mm. The largest of these abscess cavities

measured mm and extended from the paranasal region40 25

into the right cheek (figure 1D ). The subcutaneous fat layer at

the site of the abscess cavity underwent a complete necrosis.

Repeated needle punctures produced a whitish, smeary dis-

charge, a specimen of which was sent for general and specificbacterial culture and, subsequently, for virus isolation on 19

December 2000.

Approximately 6 weeks after the onset of symptoms, the

dermis in the region of the paranasal abscess became extremely

thin and was at risk of necrosis and perforation. Three punc-

tuations, which were made under general anesthesia during an

interval of 3–5 days, had no effect on the condition, and in-

cision became inevitable. Because of the risk of dermal necrosis,

hyperbaric oxygen (HBO) treatment was chosen as therapy, to

improve the chances that the infection would resolve and to

stabilize the atrophied skin before incision. The patient un-

derwent 5 courses of HBO treatments, in 6 hourly intervals,between the 21st and the 23rd of December in the pressure

chamber at the Karlskrona Naval Base.

After the first course of HBO treatment, the huge paranasal

abscess was evacuated by incision, and a drain was inserted.

The discharge diminished gradually, and the drain was removed

after 5 days. The patient’s condition quickly improved, and 6

weeks after she underwent HBO therapy and the incision, the

skin had recovered completely, including a reappearance of the

subcutaneous fat layer. However, some lymph nodes continued

to vary in size, and the bluish discoloration of the adjacent skin

areas remained. Nodes of 2–3 mm in diameter in general

showed spontaneous regression, but nodes with a diameter of 5–15 mm required needle aspirations several times, for up to

5 months after the onset of the disease. Histologic examination

of the discharge showed degenerated hyperplastic unidentifiable

cells. Examination of fine-needle biopsy specimens from the

upper jugular lymph nodes, which never necrotized, revealed

reactive lymphadenitis.

The aspirate obtained on 19 December was subjected to virus

isolation at the Department of Virology at Malmo University

Hospital (Malmo, Sweden). Ten days after inoculation on

green-monkey kidney cells, a cytopathic effect (CPE) appeared,

which, on subpassage, yielded syncytial formation of the cells.

The CPE was caused by an agent that was filterable through a

0.45-mm filter. The results of PCR and immunofluorescence

testing for mumps virus were negative.

The CPE pattern directed our suspicions to poxvirus infec-

tion, and the culture material was sent to the Swedish Institute

for Infectious Disease Control in Stockholm on 9 February 2001

for investigation for poxvirus. Orthopoxvirus-like particles

were detected in the culture medium by electron microscopy

(figure 1G ). The diagnosis was further confirmed by PCR anal-

ysis, which noted a 339-bp fragment of the viral thymidine

kinase gene, where direct sequencing revealed 100% homology

with an earlier published Swedish isolate, H2 [2]; direct se-

quencing also revealed, as expected, 99% homology with vac-

cinia virus sequences. A serum sample, which had been col-

lected 5 weeks after the onset of symptoms, was positive for

antibodies to orthopoxvirus (vaccinia virus) by plaque reduc-

tion neutralization test.The healing process of the numerous areas of lymphadenitis

was markedly prolonged. Two years after onset of symptoms,

a single firm node situated in the medial angulus of the right

eye was removed (figure 1E ). Electron microscopy evaluation

of this node yielded negative results, but PCR of the node was

positive for orthopoxvirus DNA. Sequence analysis showed to-

tal homology with the PCR product obtained from the patient

in February 2001.

Epidemiological findings. After cowpox infection was di-

agnosed (almost 3 months after the onset of symptoms), the

patient recalled having had close contact with 2 domestic cats.

One of the cats used to lick her face and nose. Close contactwith the cats was especially frequent after she came home from

the holiday in Spain. On this occasion, the cat’s tongue pen-

etrated the right nasal cavity; ∼2 weeks later, the first symptoms

appeared. No scratches were found on the girl’s nose. The cats

were in good health when examined by a veterinarian in Feb-

ruary 2001. None of them had lesions of the paws, mouth, or

nose or enlarged lymph nodes of the neck. Serum samples

obtained from both cats were tested for orthopox virus anti-

bodies at the Swedish Veterinary Institute (Uppsala), and the

results were negative.

DISCUSSION

Poxviruses are the largest enveloped DNA viruses, with an av-

erage dimension of nm. The virus particle contains230 300

a linear, double-stranded genome of 140–300 kb in length that

encodes several hundred polypeptides. Vertebrate poxviruses

contain 8 genera, of which 4 (Orthopoxvirus, Parapoxvirus,

Yatapoxvirus, and Molluscipoxvirus) contain viruses patho-

genic to humans [3], all of which, with the exception of small-

pox (variola), vaccinia virus, and molluscipoxvirus, are trans-

mitted to humans by animals (zoonosis).

Smallpox was caused by the variola virus, a member of the

Orthopoxvirus genus. It was globally eradicated in the late1970s by mass vaccination, which was successful, because the

variola virus did not have an animal reservoir. Vaccinia, known

as the “Jenner virus,” was the virus used for successful smallpox

vaccination, but the exact origin of vaccinia virus is uncertain

and there is no known natural host.

Vaccination with vaccinia virus provided cross-protection

against several orthopoxviruses, including monkeypoxvirus, the

third orthopoxvirus. Normally, vaccinia causes mild and local




Table 1. Reports on spread of orthopoxvirus in western European rodents and carnivores.

Country Mode of detection Reservoir Reference(s)

Great Britain Serologic testing and PCR Bank voles (prevalence in autumn, 80%), wood mice (prevalence, 27%),

and short-tailed field voles (Clethrionomys glareolus, Apodemus sylvaticus,

and Microtus agrestis; prevalence, 99% [11 of 12])

[5–7]

Germany Serologic testing Cats (prevalence, 2% [44 of 2173]) [8]

Nor wa y Serologic tes ting W ild c arniv ores ( red foxes [Vulpes vulpes]; prevalence, 11% [7 of 62]) and do-mestic cats (prevalence, 10.1% [n p 217])

[9]

Finland Serologic testing and PCR Rodents (mainly bank voles [Clethrionomys glareolus]; prevalence, 0%–92%,

depending on population dynamics; high prevalence during the peak phase

of population for red foxes (prevalence, 50% [7 of 14]) and lynx (preva-

lence, 1.4% [1 of 73])

[10]

Sweden Serologic testing Lynx (prevalence, 29%; [5 of 17]) and brown bears (prevalence, 2%; [1 of 45]) [10]

Germany Serologic testing Red foxes (prevalence, 6.5% [46 of 703]) [11]

Austria Serologic testing Domestic cats (prevalence, 4% [(8 of 200]) [12]

symptoms, but it may cause severe and even fatal complications

in immunocompromised individuals [1].

Monkeypoxvirus acquired attention in 1969–1970, when it

was isolated from infected humans in Congo/Zaire. Increasing

numbers of human monkeypox infections have been observed

in later years in this region of Africa, where infection occurs

in the wildlife [4].

Cowpoxvirus, the fourth orthopoxvirus—and the causativeagent of our case—is so named because it can infect the teats

of cows [2]. However, despite its name, cowpoxvirus does not

have cattle as its reservoir host; rather, rodents (such as bank

voles and wood mice) serve as its reservoir hosts [5, 6]. Car-

nivore hosts (such as cats) that hunt rodents can transmit cow-

poxvirus to humans. Serological investigations have recognized

domestic cats as the most common hosts for cowpoxvirus [7].

Antibodies against orthopoxvirus have been documented in

several rodents and carnivores; the species are shown in table

1 and are described elsewhere [5–12].

In our case, the domestic cats did not show any signs of

ongoing infection on examination, although the examination

was not performed until 3 months after exposure. Also, se-

rological investigation (immunofluorescent staining) did not

reveal antibodies to orthopoxvirus.

Human cowpoxvirus infection is a rare disease. A review of

54 cases, most of which were in the United Kingdom, indicated

that human cases coincided with autumn peaks of cowpoxvirus

infections in voles, wood mice, and domestic cats [13]. In most

of the cases involving humans, the source of the infection is

domestic cats. The infection is almost always transferred to

humans through a skin lesion, but in some cases, it is trans-

ferred via the mucosa of the eye. Infection usually starts as aninflamed macula that turns into a papule; finally, a vesicular

stage occurs within 7–12 days. The dermal vesicles become pale

blue-purple and are more or less hemorrhagic, because of cap-

illary lesions from the growth of virus in the endothelial and

pericapillary cells [14].

The lesion is usually painless, as was true for our patient,

who never complained of any pain in her nose. The lesion may

be located on the skin or mucosa, and it is typically surrounded

by marked local edema and regional lymphadenopathy, which

may be prolonged, as it was in our case. Furthermore, most of

the reported patients have slight systemic symptoms, such aspyrexia, and they sometimes experience sore throat, influenza-

like illness, and general malaise that lasts 3–10 days. The time

to complete recovery ranges from 3 to 12 weeks and can be

even longer. A selection of reported clinical features is presented

in table 2 [15–23].

Our patient had a hitherto undescribed route of inoculation

via the respiratory mucosa of the nose. The infection resulted

in a mucosal inflammation that resolved after 3 weeks. We

found necrotic material at the site of the inferior concha that

was surrounded by pebble stone-like granulations. The sub-

sequent phase was dominated by subcutaneous necrotizing

lymphadenopathy of the regional nodes; this persisted for sev-

eral months and required therapeutic needle aspirations.

The major abscess in the paranasal region covered by an

extremely thin dermis was at risk of necrosis, and the unor-

thodox decision was made to support surgical treatment with

HBO treatment. Several clinical and experimental studies have

demonstrated the usefulness of HBO treatment (e.g., the ben-

eficial effect on stimulation of granulocytes and on circulation)

[24, 25]. There was a strong clinical impression that HBO treat-

ment had a beneficial effect on the healing process (figure 1D

and 1F ). Incision of the large abscess and placement of a tem-

porary drain were also important; however, several evacuatingpunctures had been performed earlier while the patient’s con-

dition had continued to deteriorate.

Diagnosis was delayed for our patient, because the initial




Table 2. Clinical manifestations in a selection of reported cases of cowpox.

Country Year Source

Age,

years/sex of

human patients Cowpox manifestation Outcome Reference

Germany 1990 Homeless, ill cat 18/M Skin; generalization; possible lung

involvement

Immunocompromised patient

died of thromboembolism

[15]

Germany 1996 Hunting cat 11/F Neck; ulceration and regional

lymphadenitis

Rec ov er y a ft er 8 we eks [16 ]

Germany 2000 Hunting cat 11/M Cheek; skin blister and regional

lymphadenitis

Recovery after 2 months [17]

Germany 2003 Cat 36/M Eyebrow; skin blister and re-

gional lymphadenitis

Recovery within 3 weeks [18]

France 2004 Cat 11/M Sacrum; wound; cutaneous and

mucous membrane lesions

“Slow recovery” [19]

Great Britain 1996 Healthy dog 41/M Nasal tip; ulcer after scratch; bi-

lateral cervical lymphadenitis


Sweden 1990 Hunting cat 12/F Neck and skin blisters; regional

lymphadenitis

Rec ov er y a ft er 6 we eks [21 ]

Sweden 1990 Hunting cat 14/F Conjunctivitis; regional

lymphadenopathy


The Netherlands 2002 Wild rat (Rattus norvegicus) 14/F Eyelid; ulceration and regional

lymphadenitis

Rec ov er y a ft er 1 mo nt h [22 ]

Austria 2003 C at (possibly hunting) 56/F Neck, ulceration (possible

lymphadenopathy)

Rec ov er y a ft er 5 w ee ks [23 ]

Finland 2003 Patient’s dog 4/F Extremities, body, face, vulva;

generalization of atopic

dermatitis


massive cellulitis of the face resembled a H. influenzae phleg-

mon; however, the results of cultures were negative. There were

few indications pointing to a virus infection, and unfortunately,

the biopsy specimen from the nose was not sent for virological

analysis. Virus isolation from the discharge obtained 3 weeks

after hospital admission yielded a syncytium-like pattern thatwas confirmed to be orthopoxvirus by electron microscopy and

was eventually verified as cowpoxvirus by PCR and sequencing.

Although it would have been desirable to test tissue specimens

for specific viral antigens, no such tests were performed,because

the poxvirus particles and DNA that were present were unlikely

to be contaminants in an unvaccinated child. Furthermore,

examination by PCR and restriction digest performed at the

Centers for Disease Control and Prevention (Atlanta, GA) con-

firmed that the virus isolate was cowpox species.

Antibiotics (penicillin, cefuroxime, and spectramycin) were

prescribed to our patient on the basis of sparse findings of

bacterial infection and to prevent secondary infection at the

sites for puncture and incision. This therapy had no convincing

effect on the course of the disease.

At the time of diagnosis, antiviral treatment was considered.

Cidofovir is efficient against vaccinia virus infections in mice,

although it has been associated with some renal toxicity in

humans [26]. Of the other treatment options, immune globulin

was considered, as was vaccination with vaccinia virus. How-

ever, by this point in the course of infection, most of the symp-

toms had decreased, except persisting lymphadenopathy.

Most reported cases of cowpox in humans who are infected

via cats involve girls aged 12 years [17]. A tendency among

girls in this age group to cuddle cats, as in our patient, may

explain this phenomenon. Unfortunately, the patient never toldus that her cat licked her nose until we asked.

In most of the cases, the patient presents with a necrotizing

skin lesion or may have a blister with involvement of the re-

gional lymph nodes. However, if the virus has been inoculated

via a mucosal membrane (such as the eye [21] or, as occurred

in our patient, the nasal mucosa), the result may be massive

facial edema resembling erysipelas linked with lymphadenop-

athy. In such atypical cases, animal contacts and cowpoxvirus

infection should be ruled out.

Whether the abolition of smallpox vaccination in Europe

during 1971–1977 has led to an increase in the number of

cowpoxvirus infections is still a matter of discussion. During

the period of 1982–1993, Baxby et al. [13] reported 25 cases

after cessation of vaccination in 1971 in Great Britain, as well

as 20 cases during 1969–1981. Sweden reported 2 cases in 1990;

there has also been our case in 2000 and a still unreported case

in 2005. Despite a growing awareness of human cowpox in-

fection in Europe, diagnosis is certainly often missed because

cowpox infection may resemble impetigo, anthrax, or erysip-




elas; moreover, the disease often heals spontaneously within 4–

6 weeks. It is possible that only the more spectacular cases are

reported, making it difficult to estimate any increase in the rate

of human cases of cowpox after cessation of vaccination.

Acknowledgments

We are thankful for fruitful discussions with Dr. Henning Montelius

(Department of Infectious Diseases, Blekinge County Hospital, Karlskrona,Sweden) and Dr. Nils Hamnerius (Department of Dermatology, Blekinge

County Hospital). We also thank Dr. Johan Douglas (Department of An-

aesthesia) for administering effective hyperbaric oxygen therapy and Dr.

David Allen (Department of Anaesthesia) for revising the English language

test in this manuscript. We thank colleagues at the Department of Ear,

Nose, and Throat (Blekinge County Hospital; Karlskrona, Sweden) for

taking part in the surgical procedures. We also acknowledge the input of

Dr. Monica Grandien, Dr. Fredrik Elgh, and Dr. Kari Johansen (Virology

Department, Swedish Institute for Infectious Disease Control, Stockholm)

for critically reviewing the manuscript and Dr. Kjell Olof Hedlund (Virology

Department, Swedish Institute for Infectious Disease Control, Stockholm)

for performing electron microscopy.

Financial support. ALF grants from the Medical Faculty of Lund

University.

Potential conflicts of interest. All authors: no conflicts.

References

1. Mayr A, Danner K. Aufhebung der Pflichtimpfung gegen Pocken.

MMW Munch Med Wochenschr 1979; 121:1675–8.

2. Sandvik T, Tryland M, Olsvik O, Traavik T. Comparison of thymidine

kinase and A-type inclusion protein gene sequences from Norwegian

and Swedish cowpox virus isolates. APMIS 1999; 107:667–75.

3. Moss B. Poxviridae: the viruses and their replication. In: Fields BN,

Knipe DM, Howley PM, eds. Fields virology, 3rd ed. New York: Lip-

pincott Raven, 1995:2637–71.

4. Arita I, Jezek Z, Khodakevich L, et al. Human monkeypox: a newly

emerged orthopoxvirus zoonosis in the tropical rain forests of Africa.

Am J Trop Med Hyg 1985; 34:781–9.

5. Baxby D. Is cowpox misnamed? A review of 10 human cases. BMJ

1977; 1:1379–81.6. Chantrey J, Meyer H, Baxby D, et al. Cowpox: reservoir hosts and

geographic range. Epidemiol Infect 1999; 122:455–60.

7. Bennet M, Gaskell CJ, Baxby D, et al. Feline cowpox virus infection.

J Small Anim Pract 1990; 31:167–73.

8. Czerny CP, Wagner K, Gessler K, et al. Monoclonal blocking—ELISA

for the detection of orthopox virus antibodies in feline sera. Vet Mi-

crobiol 1996; 52:185–200.

9. Tryland M, Sandvik T, Mehl R, et al. Serosurvey for orthopoxviruses

in rodents and shrews from Norway. J Wildl Dis 1989; 34:240–50.

10. Pelkonen PM, Tarvainen K, Hynninen A, et al. Cowpox with severe

generalized eruption, Finland. Emerg Infect Dis 2003; 9:1458–61.

11. Henning K, Czerny C-P, Meyer H, et al. A seroepidemiological survey

for orthopox virus in the red fox. Vet Microbiol 1995; 43:251–9.

12. Nowotny N. Serologic studies of domestic cats for potential human

pathogenic virus infections from wild rodents. Zentralbl Hyg Um-

weltmed 1996; 198:452–61.

13. Baxby D, Bennet M, Getty B, et al. Human cowpox: a review based

on 54 cases 1969–93. Br J Dermatol 1994; 131:598–607.

14. Munz E, Linckh S, Renner-Muller IC. Infektionen mit originarem Ku-

hpockenvirus und kuhpockenahnlichen Erregern bei Mensch und Tier:

Eine Literaturubersicht. Zent ralbl Veterinarmed B 1992; 39:209–25.

15. Czerny C-P, Eis-Hubinger A-M, Mayr A. Animal poxviruses trans-

mitted from cat to man: current event with lethal end. Zentralbl Ve-

terinarmed B 1991; 38:421–31.

16. Stolz W, Gotz A, Thomas P, et al. Characteristic but unfamiliar—the

cowpox infection transmitted by a domestic cat. Dermatology 1996;

193:140–3.

17. Wienecke R, Wolff H, Schaller M, et al. Cowpox virus infection in an

11-year-old girl. Am Acad J J Am Acad Dermatol 2000; 42:892–4.

18. Steinborn A, Essbauer S, Marsch WC. Human cowpox/catpox infec-

tion: a potentially unrecognized disease. Dtsch Med Wochenschr2003; 128:607–10.

19. Heilbronner C, Harzic M, Ferchal F, et al. Cowpox virus infection in

a child [in French]. Arch Pediatr 2004; 11:335–9.

20. Lee WC, Manjaly G, Skinner DW, O’Neill PM. Cowpox infection of

the nose. J Laryngol Otol 1996; 110:782–4.

21. Cronquist J, Ekdahl K, Kjartansdottir A, et al. Cowpox—en kattsjuka

hos manniska. Lakartidningen 1991; 88:2605–6.

22. Wolfs TF, Wagenaar JA, Niesters HG, Osterhaus AD. Rat-to-human

transmission of cowpox infection. Emerg Infect Dis 2002; 8:1495–6.

23. Hawranek T, Tritscher M, Muss WH et al. Feline orthopoxvirus in-

fection transmitted from cat to human. J Am Acad Dermatol 2003;

49:513–8.

24. Hammarlund C, Sundberg T. Hyperbaric oxygen reduced size of

chronic leg ulcers: a randomized double-blind study. Plast Reconstr

Surg 1994; 93:829–33.25. Knighton DR, Halliday B, Hunt TK. Oxygen as an antibiotic: the effect

of inspired oxygen on infection. Arch Surg 1990; 125:97–100.

26. Donald F, Smee DF, Kevin W, et al. Intranasal treatment of cowpox

virus respiratory infections in mice with cidofivir. Antiviral Research

2000; 47:171–7.

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Cellulitis Case Tx737